GAtherton, Author at Aspergillosis Patients & Carers Support

🧬 Article 2: When Microbes Turn Hostile – The Evolutionary Pressures Behind Infection

Subtitle: Why stable colonisation sometimes shifts into active disease

Introduction

If microbes can live quietly in the lungs for years, why do they sometimes turn aggressive?
Evolutionary biology and microbiome research show that infection often develops because of environmental pressures — not by design, but as a by-product of survival in a changing ecosystem.

1. Antibiotic Pressure

Repeated antibiotic courses kill sensitive strains and leave behind resistant survivors.
These survivors often produce thicker biofilms and inflammatory molecules, which protect them but also damage airway tissue.
Over time, this selection creates harder-to-treat, more inflammatory strains.

2. Nutrient Competition

Airways are crowded ecosystems.
When nutrients run low, microbes compete by releasing toxins, proteases, and iron-scavenging molecules.
These harm competitors — and incidentally harm the lung.

3. Biofilms and Mutation

Within biofilms, bacteria and fungi evolve quickly.
Mutations can accumulate, producing hypermutator strains that are well adapted to chronic survival but also more inflammatory.

4. Host Factors

Changes in the body — reduced immunity, steroid use, diabetes, or viral infections — relax immune control.
Organisms that were previously contained can now proliferate.
Similarly, damaged or scarred airways provide sheltered niches where microbes thrive.

5. Microbiome Collapse

The healthy lung microbiome helps regulate inflammation and suppress invaders.
When broad antibiotics or infections reduce diversity, opportunists like Pseudomonas or Aspergillus can expand unchecked.

6. Collateral Damage, Not Intent

Most microbes don’t “want” to be pathogenic — they’re simply adapting to survive.
Their survival strategies (biofilms, enzymes, toxins) cause collateral damage to airway tissue.
So, pathogenicity is often an accidental consequence of survival pressure.

7. Cycles of Stability and Flare-Ups

Chronic airway diseases often follow repeating cycles:

Stable colonisation – coexistence with minimal inflammation
Disruption – antibiotics, viral infection, or new strain
Flare-up – inflammation and tissue damage
Partial recovery – new stable community forms

Each cycle leaves the microbial ecosystem slightly altered — selecting for organisms that can survive stress and immune attack.

Evolutionary Summary

Pressure	Effect on Microbes	Result for Host
Antibiotics	Resistant, stress-adapted strains	Harder-to-treat infection
Nutrient limitation	Toxin and enzyme producers	Tissue damage
Immune suppression	Less control of microbes	Opportunistic growth
Microbiome loss	Opportunist expansion	Reduced resilience
Biofilm evolution	Genetic drift, persistence	Chronic inflammation

Key Takeaway

Microbes evolve under pressure from antibiotics, immune stress, and competition.
They don’t plan to harm the host — they adapt to survive.
Unfortunately, those same adaptations often make them more damaging and persistent.

This is why good airway care, careful antibiotic use, and microbiome-friendly approaches are essential to keep the system in balance.

👉 Read also: Colonisation vs Infection in Airways Disease
(Learn how to recognise the difference, when treatment is needed, and how to keep microbial balance.)

by GAtherton

🩺 Article 1: Colonisation vs Infection in Airways Disease

Subtitle: Understanding what it means when bacteria or fungi are found in your lungs

Introduction

People with bronchiectasis, Primary Ciliary Dyskinesia (PCD), Allergic Bronchopulmonary Aspergillosis (ABPA), or Chronic Pulmonary Aspergillosis (CPA) often have microbes detected in their sputum samples.
That doesn’t always mean there’s an infection that needs treatment.
Understanding the difference between colonisation and infection helps patients and clinicians make better decisions.

Colonisation

Colonisation means that bacteria or fungi are living in the airways but aren’t currently causing harm.
This happens because mucus clearance is reduced, allowing microbes such as Haemophilus influenzae, Pseudomonas aeruginosa, or Aspergillus fumigatus to persist.

The microbes are “residents,” not invaders.
Symptoms stay stable.
Blood tests for inflammation (like CRP) are usually normal.

Treatment isn’t always needed — instead, care focuses on airway clearance, physiotherapy, hydration, and monitoring through sputum cultures.

Infection

Infection means microbes are actively causing inflammation and tissue irritation.
This happens when microbial numbers rise, new strains appear, or immune defences weaken.

Typical signs:

Increased cough, sputum, or breathlessness
Fever or feeling unwell
Raised inflammatory markers
New changes on chest X-ray or CT

Treatment involves targeted antibiotics or antifungals based on sputum results and resistance testing.

Why Colonisation Can Turn Into Infection

In chronic airways disease, colonisation and infection exist on a sliding scale — a shift in balance can push the lungs from stable to inflamed.
Common triggers include:

Growth of a new or resistant strain
Reduced mucus clearance
Viral infections (e.g. influenza, COVID-19)
Immune suppression
Loss of “friendly” bacteria in the lung microbiome

When this balance is disrupted, inflammation rises and infection takes hold.

The Balance Model

Factor	Colonisation (Stable)	Infection (Flare-Up)
Microbial strain	Stable	New or virulent
Microbial load	Controlled	Increased
Microbiome	Diverse	Reduced diversity
Immune status	Balanced	Suppressed or overactive
Symptoms	Stable	Worsening
CRP / WBC	Normal	Raised

Key Takeaway

In chronic lung conditions, microbes are often part of daily life. The aim isn’t complete eradication, but balance — keeping numbers low, reducing inflammation, and treating only when infection is active.

👉 Next article: When Microbes Turn Hostile – The Evolutionary Pressures Behind Infection
(Explore how antibiotics, competition, and disrupted microbiomes drive microbes to become more aggressive.)

by GAtherton

Living with Primary Ciliary Dyskinesia (PCD) and Bronchiectasis

People living with Primary Ciliary Dyskinesia (PCD) and bronchiectasis often face long-term challenges with their lungs. These conditions can make it difficult to clear mucus effectively, creating a perfect environment for bacteria and fungi to grow — including Aspergillus species and bacteria such as Haemophilus influenzae.

What Is Primary Ciliary Dyskinesia?

Primary Ciliary Dyskinesia is a rare, inherited condition that affects the microscopic hair-like structures (cilia) that line the airways, ears, and sinuses. Normally, cilia move in a coordinated way to sweep mucus, bacteria, and debris out of the lungs.
In PCD, these cilia don’t move properly. As a result, mucus builds up, causing chronic infections and inflammation.

How PCD Leads to Bronchiectasis

Over time, repeated infections and inflammation can damage the airways, leading to bronchiectasis — a condition where the bronchial tubes become widened and scarred. This makes it even harder to clear mucus and allows bacteria and fungi to settle in the lungs more easily.

Common organisms that may persist include:

Haemophilus influenzae
Pseudomonas aeruginosa
Staphylococcus aureus
Aspergillus fumigatus

The Role of Aspergillus

When Aspergillus spores are inhaled, most people clear them easily.
In PCD and bronchiectasis, however, mucus clearance is reduced and the airways are damaged — so Aspergillus can remain trapped.
Over time, this can lead to sensitisation (as in Allergic Bronchopulmonary Aspergillosis, ABPA) or even chronic infection (Chronic Pulmonary Aspergillosis, CPA).

Both conditions can worsen existing bronchiectasis and make bacterial infections harder to control.

Why Bacteria Like Haemophilus Stick Around

Many patients with PCD or bronchiectasis find that bacteria such as Haemophilus influenzae are always present in their sputum, even when they feel well.
This doesn’t always mean there’s an active infection — it can simply reflect colonisation (the bacteria living there without causing symptoms).
However, when bacterial numbers rise or resistance develops, this can trigger a flare-up with more cough, sputum, or breathlessness.

Managing Persistent Infections

Because eradication is often not possible, the goal is control rather than cure.
Typical strategies include:

Regular sputum cultures to monitor bacterial and fungal growth and check for antibiotic resistance.
Targeted antibiotic treatment when symptoms worsen, chosen based on recent resistance results.
Airway clearance techniques, such as physiotherapy, postural drainage, or devices that help loosen mucus.
Nebulised saline (often hypertonic) to thin mucus and make it easier to clear.
Vaccinations (e.g., flu and pneumococcal) to reduce viral triggers.
Anti-inflammatory and antifungal treatments when fungal infection or allergic sensitisation are part of the problem.
Regular monitoring with a respiratory specialist to adjust treatment plans.

Living Well with PCD and Bronchiectasis

Many people manage to live active lives by learning what works best for their lungs — combining daily airway clearance, careful infection monitoring, and prompt treatment of flare-ups.
Some also find it useful to join patient support groups, where experiences with long-term bacterial and fungal infections can be shared.

Key Takeaway

For people with PCD and bronchiectasis, infections like Haemophilus influenzae and Aspergillus fumigatus often can’t be completely removed. The focus is on keeping infection levels low, preventing flare-ups, and protecting the lungs for the long term. With good self-management, regular review, and the right treatment plan, symptoms can be controlled and quality of life maintained.

by GAtherton

🧬 From Scottish Discovery to American Pharmacy Shelf: The Story of Brensocatib

Sometimes a medicine begins life in one country but reaches patients first in another. The new bronchiectasis drug brensocatib is a perfect example — discovered in Scotland, yet first approved for use in the United States.
Here’s how that happens, and what it tells us about how new treatments make their way to patients.

1️⃣ Discovery in Dundee

At the University of Dundee, scientists in the Drug Discovery Unit (DDU) were studying how certain white blood cells called neutrophils can cause long-term lung damage.
They identified an enzyme, DPP1 (dipeptidyl peptidase I), that activates destructive substances inside these cells.
Blocking DPP1 could calm inflammation without wiping out the body’s defences.
Their research produced a promising new compound — later named brensocatib — which safely switched off this process in lab studies.

2️⃣ Partnering to Go Global

Turning an early discovery into a medicine is an enormous task.
It costs hundreds of millions of pounds and can take 10–15 years.
The Dundee team partnered with Insmed, a biotechnology company based in New Jersey, USA, which had the funding and international trial experience to move brensocatib into large clinical studies.

3️⃣ Worldwide Trials

Insmed led major trials involving hundreds of people with non-cystic fibrosis bronchiectasis in hospitals across North America, Europe, and Asia.
Results showed that brensocatib reduced flare-ups and improved quality of life.
Because Insmed’s main offices and regulatory team are in the U.S., they submitted their results first to the U.S. Food and Drug Administration (FDA).

4️⃣ U.S. Approval

In 2025, the FDA approved brensocatib — the first drug of its kind to treat bronchiectasis.
American patients can now access it while other countries complete their reviews.

5️⃣ What Happens Next in the UK

In the UK, every new medicine goes through two steps:

The Medicines and Healthcare products Regulatory Agency (MHRA) checks that it is safe and effective.
Then NICE (the National Institute for Health and Care Excellence) reviews how well it works for its cost and decides whether the NHS should fund it.

NICE is expected to make its decision on brensocatib in July 2026.
Even if approved, it may first be offered to those with the most severe or frequent flare-ups while more real-world data are gathered.

💷 What Dundee Gained from Its Discovery

Although Dundee handed over development to a U.S. company, the university continues to benefit in several ways:

Financial return: Dundee receives upfront payments, milestone fees for each stage of progress, and royalties on global sales.
These funds support new drug discovery projects, student training, and research facilities.
Scientific impact: Brensocatib’s success highlights the strength of the Drug Discovery Unit’s model, showing that UK universities can produce world-class medicines.
Future partnerships: Dundee’s achievement attracts new collaborations and investment, ensuring that more early discoveries have a route to reach patients.

So while the drug is made and sold by Insmed, Dundee’s scientists — and their reinvested funding — continue to play a role in future breakthroughs.

🏭 Manufacturing: Turning Discovery into a Real Medicine

Once a new drug is approved, it still has to be produced safely, at scale, and consistently.
This is often a completely separate operation from the research or licensing stage.

For brensocatib, the chemical process that makes the active ingredient was developed by Dundee and Insmed scientists early on, but large-scale manufacturing is now carried out by specialist pharmaceutical plants under strict international standards known as Good Manufacturing Practice (GMP).

Because brensocatib is a small-molecule oral drug (a tablet, not an injection), it’s made in high-tech chemical manufacturing facilities, not hospitals or biologics plants.
These sites are often in Europe, the U.S., or Asia, depending on where the supply chains, raw materials, and quality-control systems are strongest.

Manufacturing is expensive — it must ensure every tablet is identical in purity, strength, and safety — but it’s also where economies of scale help keep the cost manageable once global production ramps up.

For the NHS and NICE, manufacturing details matter too, because:

They affect cost-effectiveness (how much the NHS will pay per course of treatment).
They influence availability — whether the company can supply enough medicine to meet demand once approved in the UK.

So, while the discovery began in Dundee and the approval started in the U.S., manufacturing is the bridge that makes it real — transforming a scientific idea into a medicine that can be prescribed to patients worldwide.

🌍 Why This Matters

This journey shows how scientific discovery is global.
A breakthrough can start in a Scottish laboratory, be developed with American funding, tested around the world, manufactured across several continents, and eventually come back to help patients in the UK.
It’s a reminder that international collaboration — between researchers, funders, manufacturers, and regulators — is what turns good science into real treatments.

by GAtherton

🧩 NAC Aspergillosis Research Digest Aspergillosis (October 2025: week 44)

Highlights

Pulmonary aspergillosis in chronic lung disease can be severe and life-threatening, especially in patients with underlying interstitial lung conditions. Prompt diagnosis and subtype-targeted treatment are crucial for better outcomes (7).
Advanced sinus imaging in dogs improves veterinary precision for diagnosing and treating fungal infections such as aspergillosis (1).
Poultry farms in Turkey are best protected against aspergillosis outbreaks through consistent hygiene and environment management (3).
Pediatric liver transplant patients remain at high risk of deadly fungal infections, so ongoing immune and drug monitoring is vital (2).
New antifungal agents such as isavuconazole are yielding positive results in children, adults, and drug-resistant cases (10).
Agricultural fungicide use is driving azole resistance in Aspergillus, prompting urgent "One Health" responses across medicine and farming (8).
Research is underway to determine the best antifungal prophylaxis for heart transplant recipients (6).
Case studies show severe treatment challenges for aspergillosis in post-tuberculosis and cancer patients (5), (9).

Pulmonary Aspergillosis in Lung Disease

Recent research examined the prevalence and outcomes of aspergillosis among patients with interstitial lung disease (ILD) and chronic respiratory disorders. The study highlights three major forms:

Invasive Pulmonary Aspergillosis (IPA): Occurs in roughly 2% of hospitalised ILD patients, presenting with symptoms such as fever, persistent cough, and rapid decline in lung function. Those prescribed steroids or immunosuppressants and showing certain lung scan features are at greater risk. Estimated 3-month mortality can reach 50%.
Chronic Cavitary Pulmonary Aspergillosis (CPA): Represents about 0.6% of cases in target populations, with slower onset but significant respiratory impairment over time. Mortality is lower than IPA but remains notable.
Allergic Bronchopulmonary Aspergillosis (ABPA): Occurs in about 3% of studied patients, typically with a better prognosis, though delayed care can worsen outcomes.

Diagnostic strategies involve serology, antigen testing, and imaging to distinguish subtypes and select appropriate antifungal therapy. The study urges multidisciplinary care and more effective protocols for immunosuppressed patients (7).

Veterinary and Animal Health

Advanced radiological mapping now allows veterinarians to better diagnose and treat sinus aspergillosis across various breeds. This enhances surgical accuracy and supports targeted case management (1).
Poultry studies highlight aspergillosis as a leading fungal threat, with hygiene as the most effective control tactic (3).

Human Health: Transplant, Immunosuppression, and Infection

Children undergoing liver transplants require ongoing immune suppression, which increases susceptibility to severe fungal infections like aspergillosis. This underscores the value of rigorous therapeutic monitoring (2).
Current protocols are evaluating which antifungal drugs work best in heart transplant recipients to prevent invasive fungal infections (6)

Clinical Complications and Case Reports

Case studies spotlight life-threatening adrenal crisis and aspergillosis in children recovered from TB and adults with leukaemia. Timely diagnosis and combined therapies are essential for recovery (5), (9)
Transplant patients are vulnerable to bacterial and fungal sinus infections, presenting significant diagnostic challenges (4).

Drug Resistance and Novel Treatments

The rise of azole-resistant Aspergillus, driven by agricultural fungicide use, is making some forms of aspergillosis harder to treat. Integrated medical and environmental interventions are needed to slow resistance (8)
New medications, such as isavuconazole, are being adopted for severe and resistant cases in paediatric and adult populations with positive early results (10).

Reference List

by GAtherton

🏠 Awaab’s Law: What It Means for Social Housing Tenants

Awaab’s Law is one of the most important housing reforms in years.
It aims to protect tenants from damp, mould and unsafe living conditions — problems that can seriously affect health, especially for people with asthma, bronchiectasis or fungal lung disease.

The law starts to take effect in October 2025 and is named in memory of Awaab Ishak, a two-year-old who tragically died from prolonged exposure to damp and mould in a housing association flat in Rochdale.
His case led to new, legally enforceable time limits for social landlords to investigate and repair health hazards in rented homes.

📜 Where the Law Comes From

Awaab’s Law forms part of the Social Housing (Regulation) Act 2023.
It adds a new legal duty (Section 10A) to the Landlord and Tenant Act 1985, requiring every social landlord to comply with “prescribed requirements” about how quickly hazards must be investigated and repaired.

These rules are set out in the Awaab’s Law Regulations, published on GOV.UK, and enforced by the Regulator of Social Housing.

👥 Who the Law Covers

Awaab’s Law applies to:

Social landlords in England, such as housing associations and local authorities
Tenants living in social housing under secure, assured, or introductory tenancy agreements

Awaab’s Law does not yet apply to:

Private landlords or the private rented sector (PRS)
Owner-occupiers or leaseholders

The Government has confirmed that lessons from this law will inform future private-rented-sector reforms.
(Official source: GOV.UK – Awaab’s Law Guidance)

🏘️ What Is Social Housing?

Social housing is housing owned or managed by public or not-for-profit organisations and rented out at below-market rates to people in housing need.
It provides secure, long-term homes and is regulated by the Regulator of Social Housing.

(Official source: Regulator of Social Housing – GOV.UK)

🧱 Who Provides It

Local authorities (councils) – council housing
Housing associations – independent, not-for-profit registered providers
Charitable or community landlords – smaller providers that must still meet national standards

These organisations are known as registered providers under the Housing and Regeneration Act 2008.

💰 How Social Housing Differs from Other Tenancies

Feature	Social Housing	Private Rented Housing	Shared Ownership / Leasehold
Who owns it	Council / housing association	Private landlord / company	Part tenant part provider
Rent level	Below market (50–80%)	Market rate	Rent on unsold share + mortgage
Tenancy type	Secure / assured (long-term)	Assured shorthold (short-term)	Leasehold ownership
Regulation	Regulator of Social Housing	Local authority & housing law	Leasehold law
Repair standards	Decent Homes Standard + Awaab’s Law	General HHSRS duties	As defined in lease
Who qualifies	Based on housing need	Anyone meeting market criteria	Specific financial criteria

⚙️ What Landlords Must Do Under Awaab’s Law

Social landlords must:

Investigate reported hazards quickly
Provide written findings after inspection
Repair and make safe within legal deadlines
Offer temporary accommodation if the home cannot be made safe in time

These duties cover damp and mould and any emergency hazard posing serious risk to health or safety.

🕒 Timeframes Landlords Must Follow

Stage	Time Allowed	Example
Emergency hazard	Make safe immediately / within 24 hours	Gas leak, severe mould, electrical fault
Significant hazard	Investigate within 10 working days	Damp, cold, structural issues
Tenant update	Written summary within 3 working days	Explain findings + repairs
If not safe in time	Provide alternative accommodation	Until repairs complete

(Source: GOV.UK – Draft Guidance)

💬 Why Mould and Damp Matter

Damp and mould are common and dangerous in UK housing and can worsen or trigger asthma, ABPA, CPA, and COPD.
The English Housing Survey (2023) found 1 in 10 social homes had damp or mould problems.

Mould exposure can cause:

Asthma flare-ups and new respiratory infections
Worsening of fungal lung disease
Eye, throat, and skin irritation

Awaab’s Law recognises that poor building design and ventilation, not “tenant lifestyle,” are usually to blame.

🏘️ Why Shared and Multiple-Occupancy Homes Are Higher Risk

Buildings converted into Houses in Multiple Occupation (HMOs) are prone to damp and mould because they:

House many people in small spaces
Were often converted without proper ventilation or insulation
Rely on multiple tenants to report and manage repairs

HMOs are mainly in the private rented sector and not covered by Awaab’s Law.
They are regulated separately under the Housing Act 2004 and inspected by councils using the Housing Health and Safety Rating System (HHSRS).

These homes frequently house students, low-income workers, and people with chronic illness, making damp-related respiratory illnesses a particular concern.

🧱 Why HMOs Need Stronger Oversight

Local authorities can issue Improvement Notices or prosecute landlords for neglecting repairs, but Awaab’s Law’s fixed deadlines do not yet apply.
Government statements indicate future reforms will extend similar protections to private and HMO tenants.

💬 Why This Matters for Health

For anyone with chronic lung disease (ABPA, CPA, asthma, bronchiectasis), damp and mould can trigger flare-ups and new infections.
Awaab’s Law now forces social landlords to act promptly within set legal time limits.

Tenants can:

Use the landlord’s complaints procedure
Contact the Housing Ombudsman Service
Report serious risks to the Regulator of Social Housing or local council

🏛️ Does Awaab’s Law Apply to MOD, NHS, and Other Service Housing?

No — not directly.
Awaab’s Law covers registered social housing providers in England (local authorities and housing associations).
It does not extend to housing owned or managed by the Ministry of Defence (MOD), NHS Trusts, or other public-service employers, unless they are formally registered social landlords (which is rare).

Housing Type	Covered by Awaab’s Law?	Notes
Council / Housing Association Homes	✅ Yes	Registered providers under the Regulator of Social Housing
Private Rented Sector	❌ No (not yet)	May be included in future reforms
MOD (Service Family Accommodation)	❌ No	Managed by Defence Infrastructure Organisation; standards set by policy, not law
NHS Staff Accommodation	❌ No	Governed by occupational licence terms and health & safety law
University or Key Worker Housing	❌ No	Treated as private or institutional housing
Charitable / Supported Housing	⚠️ Sometimes	Only if registered with the Regulator of Social Housing

These providers must still maintain safe conditions under Health and Safety law, but they do not yet have the same legal repair timescales as social landlords.
The Government has stated that principles from Awaab’s Law may be used to improve MOD and NHS housing standards in future.

(Sources: legislation.gov.uk, GOV.UK – Awaab’s Law Guidance, Parliament.uk HCWS423)

🧩 Summary

Key Point	What It Means
Who it covers	Tenants in social housing (England only)
What it covers	Damp, mould, and serious health hazards
When it starts	From 27 October 2025
Who it excludes	Private, MOD, NHS and service housing
Why it matters	Protects tenants from unsafe homes and poor health
Who enforces it	Regulator of Social Housing / Local Authorities
Official sources	GOV.UK / legislation.gov.uk / Parliament.uk

🔗 Official References

by GAtherton

🌿 Will My Body Start Making Cortisol Again After Long-Term Prednisolone?

Many people with Allergic Bronchopulmonary Aspergillosis (ABPA) take prednisolone (a corticosteroid) for long periods to control inflammation and prevent flare-ups.
A common concern is whether the body will ever start producing its own natural steroid hormone, cortisol, again after so many years of treatment.

💡 Why Cortisol Matters

Cortisol is a vital hormone made by your adrenal glands.
It helps your body manage stress, maintain healthy blood pressure, control inflammation, and balance energy levels.
Your brain normally regulates this through the HPA axis (Hypothalamus–Pituitary–Adrenal axis).

When you take prednisolone, your body senses there’s already enough steroid circulating, so your brain switches off the signal that tells the adrenals to make cortisol.
Over time, the adrenal glands can “go to sleep”.

⏳ After Long-Term Prednisolone Use

If you’ve taken prednisolone for months or years, your adrenal glands may not restart immediately — and sometimes not completely.
Recovery depends on several factors:

Factor	How It Affects Recovery
Length of treatment	The longer you’ve been on steroids, the slower recovery tends to be
Average daily dose	Higher doses suppress the adrenal glands more strongly
Tapering speed	A gradual, careful reduction helps the adrenals “wake up” again
Individual differences	Some people recover in months, others may need lifelong steroid replacement (hydrocortisone tablets)

📅 What to Expect

After short courses (a few weeks), cortisol production usually returns quickly.
After many months or years, recovery can take months or even years.
Some people never regain full adrenal function and need lifelong replacement therapy.

Your specialist will usually assume your adrenal glands are suppressed until tests prove otherwise.

⚠️ Why Adrenal Suppression Is a Safety Concern

If your adrenal glands are not producing cortisol and you suddenly stop prednisolone, or become ill, have an accident, or need surgery, your body can’t produce the extra steroid it needs to handle stress.
This can cause a serious medical emergency called adrenal crisis, which may lead to low blood pressure, collapse, or shock if untreated.

That’s why it’s vital to:

Carry a Steroid Emergency Card or Medical Alert bracelet at all times
Tell healthcare staff (doctors, dentists, pharmacists, A&E teams) that you’re on or recently stopped steroids
Never miss a dose and never stop suddenly without medical advice
Use “stress-dose” steroids during illness, surgery, or injury as advised by your doctor

These simple precautions can be life-saving if your body can’t make enough cortisol during stress.

💨 What About Inhaled Steroids?

Many people with ABPA or asthma also use inhaled corticosteroids (such as fluticasone, budesonide, or beclometasone) in combination inhalers like Seretide, Symbicort, or Fostair.
These medicines mainly act in the lungs and only a small amount enters the bloodstream — but at high doses or with long-term use, they can still partly suppress the adrenal glands, especially when combined with oral steroids or certain antifungal medications.

Adrenal suppression is more likely if:

You use high-dose inhaled steroids for many months or years (e.g. fluticasone >500 µg/day)
You also take oral steroids (even at low doses)
You’re on antifungal medicines such as itraconazole, voriconazole, or posaconazole, which slow steroid breakdown
You are particularly sensitive to steroid effects

If suppression occurs, you might feel unusually tired, dizzy, or weak — especially when unwell or under stress.

Your doctor may test your morning cortisol or do a Synacthen test if there’s any concern.
In some cases, patients on high-dose inhaled therapy are also advised to carry a steroid card for safety, just like those on oral steroids.

The good news is that inhaled steroids are much safer than long-term oral prednisolone, and the risk of serious adrenal problems remains low when used correctly.

🧪 How Doctors Check for Recovery

Your respiratory or endocrine team may arrange:

Morning cortisol blood test (before your usual dose)
ACTH stimulation test (Synacthen test) – to see how well your adrenal glands respond

These tests help guide your doctors in determining whether your body is producing enough cortisol naturally or if you require a maintenance or replacement dose.

💊 Why Some Patients Move from Prednisolone to Hydrocortisone

If you’ve been on long-term prednisolone and your body is no longer making enough cortisol, your doctor may switch you to hydrocortisone.
Hydrocortisone is almost identical to the natural cortisol your body should produce.

Feature	Prednisolone	Hydrocortisone
Strength	4–5 times stronger than cortisol	Matches the body’s natural cortisol
Duration of action	Long-acting (12–36 hours)	Short-acting (6–8 hours)
Typical use	Controls inflammation during flares	Replaces missing cortisol when adrenals are suppressed

Hydrocortisone is used as replacement therapy, not as an anti-inflammatory drug.
It’s given when your adrenal glands are “asleep” after long-term steroid use — or permanently if they no longer recover.

Doctors may switch to hydrocortisone if:

Tests show adrenal suppression (low morning cortisol or poor Synacthen test results)
You’ve finished tapering off prednisolone, but still feel unwell or fatigued
You have symptoms of adrenal insufficiency, such as dizziness, nausea, or low blood pressure
You need more precise stress dosing during illness or surgery

Hydrocortisone more closely mimics the body’s natural rhythm, usually taken two or three times a day, with an increased dose during illness or stress.

If you’re on hydrocortisone:

Carry a Steroid Emergency Card and make sure it’s visible to healthcare staff.
Never stop suddenly.
Increase (“double”) your dose when you’re ill or having surgery, as advised by your doctor.
Seek urgent medical help if you vomit and can’t keep tablets down — you may need an injection.

For many ABPA patients, hydrocortisone is temporary, helping to support the body until natural cortisol production recovers.
In others, especially after many years of prednisolone, it may become a lifelong replacement, which is safe and well managed under specialist supervision.

💉 The Future: Reducing Dependence on Prednisolone

The good news is that newer treatments called biologics are changing how ABPA is managed.
Biologics such as mepolizumab, benralizumab, dupilumab, and omalizumab target specific immune pathways involved in ABPA rather than suppressing the whole immune system.

For many patients, biologics:

Reduce or replace the need for long-term steroids
Lower the risk of adrenal suppression
Control symptoms more precisely, with fewer side effects

This means more people with ABPA may, in the future, safely taper off prednisolone and give their adrenal glands a chance to recover — always under close medical supervision.

🌤️ In Summary

After many years on prednisolone for ABPA, some people’s adrenal glands do recover, while others remain partially or fully dependent on replacement steroids.
Recovery is slow, varies between individuals, and must be guided by your specialist.
Be aware that both oral and inhaled steroids can suppress the adrenals if used long-term or at high doses.
Carrying a steroid emergency card and knowing what to do in an emergency is essential for safety — especially while your adrenals are still “waking up.”
With newer treatments like biologics and careful follow-up, the goal is to reduce steroid dependence and protect your long-term health.

by GAtherton

🧠 Can Aspergillosis Spread to the Brain?

You may have read headlines saying “Aspergillosis can spread to the brain and is one of the world’s deadliest fungal infections.”
That sounds frightening — but here’s what’s really known.

💬 The truth behind the headline

It’s true that the Aspergillus fungus can affect the brain, but this is very rare and happens only in people who are severely unwell or have very weak immune systems (for example, after chemotherapy, bone-marrow transplant, or very high-dose steroids for long peroids).

For most people with aspergillosis — whether allergic (ABPA) or chronic (CPA) — the infection stays in the lungs or sinuses. These forms do not usually spread to other parts of the body.

⚙️ How brain infection can happen

When it does occur, the fungus can reach the brain in two ways:

Through the bloodstream — from an invasive infection in the lungs.
By direct spread from the sinuses — through the bone between the sinuses and the brain.

These situations are very unusual and normally occur in patients whose immune defences are severely damaged.

📉 How common is it?

CNS (brain) aspergillosis makes up only a small fraction of all cases worldwide.
Even in high-risk hospital patients, it affects fewer than 1 in 10 people with invasive aspergillosis.
In people with allergic or chronic forms like ABPA or CPA, it’s almost unheard of.

❤️ What this means for you

If you have ABPA or CPA, the fungus in your lungs is not invading tissue in the same way.
It causes inflammation, allergy, or slow-growing cavities, but not deep invasion into blood vessels or brain tissue.
So, the risk of it spreading to the brain is extremely low.

Keep up with your usual care, medications, and check-ups — these control the lung disease and help prevent complications.

⚠️ When to seek medical advice

Contact your doctor urgently if you ever notice:

New or severe headaches
Changes in vision
Seizures or sudden weakness
Confusion or loss of balance

These symptoms are not common, but they’re always worth checking.

✅ Bottom line

The media headline is partly true — aspergillosis can reach the brain, but this happens almost only in people who are very immunocompromised.
For patients with ABPA or CPA, it is extremely rare and not something to fear day-to-day.

by GAtherton

🌧️ Damp Homes and Aspergillosis: Why This Matters

Damp homes

If you live with aspergillosis, asthma, or other chronic lung conditions, your home environment plays a vital role in how well you stay.
Dampness, mould, and poor ventilation allow fungi — including Aspergillus — to grow and release spores into the air. Breathing in these spores can irritate airways, trigger allergic reactions, or worsen infection risk.

That’s why the NAC CARES team has gathered the latest UK policy, research, and practical guidance on this issue — all now available on our new information hub:
👉 Damp Homes – UK Policy and Research

🏠 What’s New on the Aspergillosis.org Damp Homes Page

Over the past week, the NAC CARES team has published a series of new articles and updates that help you:

1. Understand the Health Risks

How damp and mould can worsen breathing symptoms or trigger flare-ups in conditions like Chronic Pulmonary Aspergillosis (CPA) and Allergic Bronchopulmonary Aspergillosis (ABPA).
Why people with weakened lungs or immune systems are especially at risk.
The hidden signs of mould exposure — condensation, musty odours, or discoloured walls — even when no visible black mould is seen.

2. Learn About Your Rights and What to Do

What to check if you rent your home and find damp or mould.
Step-by-step guidance on how to report problems, who is responsible for fixing them, and what help is available if landlords or councils don’t act.
Links to official UK guidance, including the Awaab’s Law updates, which strengthen tenants’ rights to safe housing.

3. Keep Up with the Latest Research and Policy

Summaries of recent UK housing and health studies connecting damp homes to respiratory illness.
Insights into national policy changes — including new housing safety standards and public health responses.
Easy-to-read summaries of scientific studies showing how mould affects airways and immune response in vulnerable patients.

🧰 How to Use the New Page

Start with the main hub: Damp Homes – UK Policy and Research.
This gathers all the latest NAC CARES articles, research links, and resources in one place.
Explore by topic:
- Health & Risk – what damp means for your lungs.
- Practical Advice – how to spot and deal with mould.
- Policy & Research – what the UK government and researchers are doing to address the problem.
Take action:
Use the linked materials when talking with your GP, local council, or housing officer. Having official NHS and government evidence can help you get faster results.

💬 Key Takeaways for Aspergillosis Patients

Keep your home dry, warm, and well-ventilated.
Report damp or mould promptly to landlords or housing providers — and keep written records.
If your symptoms worsen and you suspect environmental triggers, speak with your care team at NAC or your respiratory specialist.
Use the NAC CARES Damp Homes page as a trusted, evidence-based guide to understanding your risks and your rights.

by GAtherton

🌬️ Inhaled Antifungal Treatments for Chronic Pulmonary Aspergillosis (CPA)

Updated: October 2025

💡 Why are inhaled antifungals being developed?

For people living with Chronic Pulmonary Aspergillosis (CPA), treatment usually involves long courses of oral antifungal tablets such as itraconazole, voriconazole, or posaconazole.
These medicines circulate through the whole body to reach the lungs — but sometimes they cause side-effects, interact with other drugs, or fail to reach high enough levels in thick mucus, cavities, or scarred areas of lung tissue.

Inhaled antifungal therapy aims to solve this problem by delivering medicine directly to the lungs using a nebuliser or inhaler device.
This can potentially mean:

✅ Higher drug levels exactly where infection is active
⚡ Faster local action
🚫 Fewer whole-body side-effects
🧩 Fewer drug interactions

This approach is especially promising for patients with localized lung disease, such as CPA or aspergillus bronchitis, where the fungus lives in damaged parts of the lung.

💊 Current inhaled antifungal options (used off-label)

🧪 Nebulised Amphotericin B

At the moment, nebulised amphotericin B is the only inhaled antifungal used in hospitals, although it is off-label for CPA.

It is more commonly used to prevent infection in people who have had a lung transplant or who are severely immunocompromised.
In some specialist centres, it may be used as maintenance therapy or an add-on for CPA if other antifungals have not worked or cannot be tolerated.

Advantages

High concentration in lung tissue
Minimal effects on other organs (especially the kidneys)

Drawbacks

Possible airway irritation (cough, tight chest, wheezing)
Requires specialist supervision and appropriate nebuliser equipment

🔬 New treatments in development

💨 Opelconazole (also called PC-945)

Opelconazole is a new inhaled triazole antifungal developed by Pulmocide Ltd in the UK.
It works in the same way as existing azole antifungals — by blocking the fungal enzyme CYP51 — but has been specially designed to stay in the lungs and minimise side-effects elsewhere.

In laboratory and early human studies, opelconazole has shown:

Strong activity against Aspergillus fumigatus
High and lasting drug levels in the lungs
Very low blood levels (reducing risk of toxicity and drug interactions)
Good tolerability in early trials

Although not yet licensed, it has been used compassionately in small numbers of patients with difficult-to-treat lung aspergillosis at centres such as Manchester and London.

🧾 Current and recent clinical trials

Trial ID	Treatment	Condition	Purpose / Summary	Status
NCT06447402	Nebulised Amphotericin B vs Saline	Chronic Pulmonary Aspergillosis	Tests whether regular nebulised amphotericin can help prevent CPA relapse compared with saline.	Recruiting
NCT03656081	Itraconazole ± Nebulised Liposomal Amphotericin B	CPA	Compares oral itraconazole alone versus itraconazole plus inhaled amphotericin for symptom and scan improvement.	Completed – results pending
NCT05238116	Inhaled Opelconazole + Standard Therapy	Refractory Invasive Pulmonary Aspergillosis	Phase 3 trial evaluating safety and added benefit of inhaled opelconazole. UK, EU, and US sites.	Recruiting
NCT05037851	Inhaled Opelconazole (PC-945)	Post-Lung Transplant Prophylaxis	Assesses prevention of fungal infection after transplant. Found well tolerated.	Completed
PubMed 34058036	Nebulised Amphotericin B vs Oral Itraconazole	Pulmonary Aspergilloma (CPA subset)	Six-month open study found similar improvement rates between inhaled amphotericin and oral itraconazole.	Completed

👉 You can look up any of these studies on ClinicalTrials.gov by entering the trial ID (e.g. NCT06447402).

⚠️ Things to keep in mind

Not yet routine — Inhaled antifungals are available only in research or specialist centres.
Limited evidence — Most data come from transplant or invasive aspergillosis studies, not chronic infection.
Delivery challenges — Damaged or scarred areas of lung may be hard for inhaled drugs to reach.
Possible side-effects — Coughing or mild bronchospasm are common; pre-treatment with an inhaler may help.
Monitoring still needed — Even with inhaled therapy, your care team will continue to check symptoms, lung scans, and blood markers (such as Aspergillus IgG).

🧭 Questions to ask your specialist

If you are interested in this type of therapy, you could ask:

Does my centre offer nebulised amphotericin as part of CPA care?
Are there any clinical trials nearby (for example NCT06447402 or NCT05238116)?
Could an inhaled antifungal be used with my current oral treatment?
What are the side-effects and how are they monitored?
What nebuliser device is required and how often would I use it?

🏥 UK research centres involved

Current UK involvement is mainly through:

National Aspergillosis Centre, Wythenshawe Hospital (Manchester)
Royal Brompton and Harefield Hospitals (London)
UK transplant centres participating in Pulmocide’s opelconazole studies

🗝️ Key takeaway

Inhaled antifungal medicines are an exciting development that could make CPA treatment safer and more targeted in the future.
For now, they are mainly available through clinical trials or specialist centres, but the early results are promising — especially for those who have struggled with oral antifungal side-effects or limited success.

If you’re interested, speak to your CPA specialist or the National Aspergillosis Centre team about ongoing research and eligibility.

by GAtherton