Biofilms: what they are, why they cause persistent infection, and how research is changing treatment

1. What exactly is a biofilm?

A biofilm is a structured community of microbes—bacteria, fungi, or a mixture—that attaches to a surface and produces a self-generated protective matrix.

The building blocks

Biofilms contain:

Cells: e.g., Aspergillus fumigatus, Pseudomonas aeruginosa, Staphylococcus aureus
Extracellular polymeric substances (EPS):
- Sticky sugars (polysaccharides)
- Proteins
- DNA released from dead cells (eDNA)
- Lipids
  These form the thick “slime” layer.

Microbial ‘specialisation’

Within a biofilm, microbes change behaviour:

Some become slow-growing persister cells, which survive drug exposure.
Others produce signalling molecules (“quorum sensing”) to coordinate defence systems.
The deeper layers become low-oxygen and acidic, making antifungals and antibiotics less effective.

Where do biofilms form in lung disease?

In bronchiectatic airways, where mucus stagnates
Around Aspergillus cavities in chronic pulmonary aspergillosis (CPA)
In mucus plugs in ABPA
In sinuses of patients with chronic fungal sinusitis
On medical devices (catheters, stents)

2. Why biofilms create so many problems

Biofilm problem 1: Immense drug resistance

Microbes in biofilms can be 100–1,000× more tolerant to antifungals/antibiotics.
This is due to:

EPS matrix blocking drug penetration
Slow metabolic rate → drugs that target growth become less effective
Persister cells surviving even high doses
Enzymes in the biofilm breaking down drugs

Aspergillus biofilms show increased resistance to:

Azoles (itraconazole, voriconazole)
Amphotericin B
Echinocandins to a lesser extent

Pseudomonas biofilms resist:

Ciprofloxacin
Colistin (partially)
Beta-lactams
This helps explain your recent comment about Pseudomonas now being resistant even though you haven’t used ciprofloxacin for years—biofilms drive spontaneous resistance through evolution, stress responses, and gene exchange.

Biofilm problem 2: Immune evasion

Immune cells (neutrophils, macrophages) cannot easily penetrate the EPS layer.
This leads to:

Incomplete clearance → long-term infection
Chronic inflammation → lung damage, fatigue
Continuous mucus production triggered by inflammation

For Aspergillus, the fungus can switch genes on/off to avoid immune detection when it grows as a biofilm-like sheet rather than as airborne spores.

Biofilm problem 3: Mixed infections behave differently

When bacteria and fungi coexist, they interact:

Pseudomonas produces molecules that stimulate Aspergillus regrowth, or vice versa
Each organism’s biofilm strengthens the other
Mixed biofilms activate more intense inflammation
They can shift the entire lung microbiome into a more disease-promoting “ecology”

This is why people with bronchiectasis or ABPA often experience:

Frequent exacerbations
Slow recovery
Mucus plugging
Worsening lung function over time

3. Why people with aspergillosis and bronchiectasis are especially vulnerable

Stagnant mucus

Biofilms love:

Thick mucus
Low airflow
Damp surfaces

All of which are present in:

Bronchiectasis
ABPA (due to mucus plugging)
Chronic pulmonary aspergillosis
Severe asthma with fungal sensitisation (SAFS)

Altered immunity

Long-term steroid use, high IgE, eosinophilia, and chronic inflammation all influence how readily biofilms form and how well the immune system can clear them.

Frequent antibiotic/antifungal exposure

This shapes the microbial community in a way that makes biofilms more likely and more resistant.

4. What we are doing to tackle biofilms

A. Current clinical strategies

1. Airway clearance is the single most effective biofilm disruptor

Physiotherapy techniques that help:

ACTs (Active Cycle of Breathing Techniques)
Oscillating devices (Flutter, Acapella)
Postural drainage
Autogenic drainage
Saline nebulisation

These physically remove biofilms, which no drug can fully achieve alone.

2. Nebulised therapies

Hypertonic saline (3–7%) helps break down mucus and destabilise the EPS matrix
Inhaled antibiotics (tobramycin, colistin, aztreonam) target bacterial biofilms
Nebulised antifungals are being explored, though not yet standard care

3. Anti-inflammatory control

Steroids/biologics help reduce airway swelling and mucus stasis, indirectly reducing biofilm formation.

4. Managing comorbidities

Reducing reflux
Improving sinus clearance
Treating asthma aggressively

All reduce the “fuel” available to biofilms.

B. Research and innovation

1. New antifungals with anti-biofilm activity

Olorofim
Fosmanogepix
Ibrexafungerp

These show better penetration and less susceptibility to biofilm-related resistance.

2. Quorum sensing blockers

Compounds that prevent microbes from “communicating” so they cannot coordinate a biofilm. In trials for Pseudomonas.

3. Enzymes to dissolve the biofilm matrix

Research into:

DNases
Polysaccharide-breaking enzymes
Surfactants

These aim to weaken the EPS “scaffolding”.

4. Microbiome-based approaches

Understanding how lung microbial ecosystems shift in disease could allow:

Removal of harmful species
Strengthening protective species
Reducing biofilm formation overall

5. Combination therapies

Antifungal + antibiotic + mucolytic
is likely the future for patients with mixed fungal–bacterial biofilms.

5. Key takeaways

Biofilms are highly organised microbial fortresses that are difficult for drugs and the immune system to reach.
They cause persistent infection, inflammation, and drug resistance.
In aspergillosis and bronchiectasis, they play a central role in ongoing symptoms and flare-ups.
Airway clearance remains the cornerstone of treatment today.
New antifungals, antibiofilm agents, and microbiome therapies offer real hope for breaking biofilm-related disease cycles.

by GAtherton

Advisory note: Preventing shingles for people with aspergillosis (ABPA, CPA, SAFS, severe asthma)

People living with aspergillosis often have additional factors that can increase the chance of shingles. The good news is that most of the risk can be reduced with vaccination, good overall health management, and early treatment of flares.

⭐ 1. Why people with aspergillosis may be at higher risk

Several common parts of ABPA/CPA management can slightly increase the chance of shingles:

🔸 Long-term or repeated oral steroids

(e.g., prednisolone, methylprednisolone, hydrocortisone)

Steroids suppress parts of the immune system, making it easier for the varicella-zoster virus to reactivate.
Even short courses can temporarily raise the risk.

🔸 Biologic treatments

(e.g., omalizumab, benralizumab, dupilumab, tezepelumab)

Biologics do not massively weaken immunity, but they do adjust key immune pathways and may slightly increase susceptibility to viral reactivation in some people.
For most patients the risk is small — but it still supports the case for vaccination.

🔸 Long-term lung disease (CPA, bronchiectasis, ABPA)

Chronic inflammation and repeated infections place extra strain on the immune system.
Many patients also experience fatigue and poor sleep, which contributes.

🔸 Other health factors

Older age (risk rises sharply after 50)
Diabetes
Nutrient deficiencies (low vitamin D, B12, folate, iron)
Recent infection, hospitalisation or surgery
High stress levels or poor sleep

⭐ 2. Vaccination — your strongest protection

The UK uses Shingrix, a non-live vaccine, safe for nearly all patients with aspergillosis, including those on:

✓ Long-term steroids
✓ Antifungals (itraconazole, voriconazole, posaconazole, isavuconazole)
✓ Biologics
✓ Immunosuppressants
✓ Long-term antibiotics for bronchiectasis

How long does protection last?

Very high protection for at least 10 years
~80–85% protection still present at year 10
No booster currently recommended

If you're over 50, or at higher risk due to medications or immune status, you are usually eligible.

⭐ 3. What else you can do

🔸 Keep inflammation under control

Flares of ABPA, CPA progression, chest infections or sinusitis all place extra strain on the immune system.
Early treatment helps reduce shingles risk.

🔸 Protect your general immunity

Good sleep
Pacing and avoiding exhaustion
Managing stress where possible
Eating routinely and correcting low nutrients (vitamin D, B12, folate, iron)

🔸 Keep up with preventive routines

Airway clearance
Prompt treatment of infections
Attending monitoring appointments
Keeping antifungal or biologic treatment stable where possible

⭐ 4. Know the early warning signs

Early treatment with antivirals works best if started within 72 hours.

Pain, tingling, burning or heightened sensitivity in a band or patch
Followed by a rash or blisters on one side of the body or face

Seek GP/urgent care the same day.

⭐ Summary for aspergillosis patients

You may be at slightly higher risk of shingles if you:

Take oral steroids
Use biologic injections
Have CPA, ABPA, bronchiectasis or long-term lung inflammation
Have low immunity, poor sleep, or ongoing infections

You can significantly reduce your risk by:

Getting the Shingrix vaccine if eligible
Managing flares and infections promptly
Supporting your immune system through sleep, pacing and nutrition
Acting early if symptoms of shingles appear

by GAtherton

**Adrenal Insufficiency & Steroid Tapering:

A Complete Patient Guide**

People taking long-term steroids (prednisolone, methylprednisolone, hydrocortisone, dexamethasone) can develop adrenal insufficiency because their adrenal glands “go to sleep” and stop making cortisol.
During tapering, the body must slowly “wake up” again — and this needs careful monitoring.

This guide explains the symptoms, tests, warning signs, and emergency precautions to keep you safe.

⭐ 1. Why adrenal insufficiency happens

Long-term steroid use suppresses the HPA axis (hypothalamus–pituitary–adrenal system).
When daily steroid doses are reduced, your body must produce more of its own cortisol. This takes time.

If the steroid reduction is too quick, or the body is under stress, low cortisol symptoms appear.

⭐ 2. Symptoms to watch for during steroid tapering

These are early signs that your body may not be keeping up with the reduction.

✔ Early, mild symptoms

Fatigue / sudden exhaustion
Muscle weakness
Dizziness when standing
Nausea or reduced appetite
Flu-like aching
Low mood, anxiety, irritability
Brain fog
Feeling unusually cold
Worsening joint or muscle pain

These often improve if the taper is slowed or paused.

⭐ 3. More serious symptoms of low cortisol

These symptoms suggest steroid levels are too low and the taper needs urgent review:

Vomiting
Persistent dizziness
Very low blood pressure
Severe fatigue (unable to function normally)
Salt cravings
Ongoing nausea preventing eating
Faintness or near-collapse

These require medical advice (same day).

⭐ 4. Emergency symptoms — possible adrenal crisis

Call 999 or go to A&E immediately if you develop:

Severe vomiting or diarrhoea
Collapse or inability to stand
Severe dehydration
Confusion
Sudden severe abdominal or back pain
Pale, clammy skin
Rapid breathing
Loss of consciousness

This is a medical emergency.
Patients normally receive 100 mg hydrocortisone IM/IV, but patients allergic to hydrocortisone require a pre-agreed emergency alternative — your endocrinologist must document this clearly.

⭐ 5. Symptoms that mean you may need a temporary “stress dose” of steroids

Your cortisol requirement increases during physical stress.
If you have adrenal suppression, your body cannot produce this extra cortisol.

You may need a temporary increase in dose if you have:

✔ Illness

Fever
Chest infection
Flu-like illness
COVID
Urinary infection
Gastroenteritis
Diarrhoea
Persistent nausea

✔ Physical stress

Injury
Significant fall
Severe pain
Dental surgery
Medical or surgical procedures

✔ Emotional stress

Bereavement
Panic attacks
Trauma

If vomiting prevents taking steroids → seek emergency help immediately.

⭐ 6. Tests used to monitor adrenal function during tapering

Doctors rely on a combination of symptoms and laboratory tests.

✔ Morning cortisol (8–9 am)

A key test to assess recovery.

Typical interpretation:

> 400–500 nmol/L → likely normal function
150–350 nmol/L → recovering / borderline
< 100 nmol/L → adrenal insufficiency

(Exact thresholds vary.)

✔ ACTH level

Shows whether the pituitary is trying to stimulate the adrenals.

Low ACTH → still suppressed
High ACTH → trying to wake adrenals
Normal ACTH + low cortisol → gland slow to respond

✔ Short Synacthen Test (SST)

Gold standard.
A small ACTH injection tests whether your adrenal glands can produce cortisol.

Used when:

taper reaches low doses
symptoms appear
deciding if steroids can be stopped

✔ Electrolytes (U&Es)

Low cortisol may cause:

Low sodium
High potassium (less common in steroid-induced insufficiency)

✔ Blood pressure monitoring

Low cortisol → low BP, dizziness, faintness.

✔ Glucose levels

Low-normal glucose and shakiness may occur during withdrawal.

✔ Clinical symptom review

Symptoms are sometimes more sensitive than tests.

Doctors track:

fatigue
appetite
dizziness
illness triggers
salt cravings
mental state
recovery after small dose increases

⭐ 7. How tapering decisions are made

Tapering depends on:

how long steroids have been taken
current dose
symptoms
test results
presence of illness
rate at which symptoms develop
allergy restrictions (pred/hydrocortisone allergy requires specialist handling)

General principles (not schedules):

Higher doses can reduce more quickly.
Taper slows dramatically near physiological levels
(~4–6 mg pred-equivalent).
If symptoms appear → pause, slightly increase, or slow taper.
SST is used near the end to confirm recovery.

⭐ 8. When to contact your medical team

Same day advice needed

worsening dizziness
persistent nausea
new vomiting
symptoms appear with each taper step
fainting
new severe fatigue
any infection (urinary, chest, flu)

Urgent / A&E

collapse
severe vomiting/diarrhoea
confusion
severe abdominal pain
unable to take oral steroids
suspected adrenal crisis

⭐ 9. What patients should do to stay safe

Carry a Steroid Emergency Card at all times
Keep emergency instructions from your endocrinologist
Know your Sick Day Rules
Ensure A&E or ambulance crews know about corticosteroid allergy
Keep a written record of tapering plan
Never stop steroids suddenly
Be cautious during illness
Know your emergency steroid plan (alternative if allergic to hydrocortisone)

⭐ Final reassurance

Adrenal insufficiency during tapering is common, manageable, and often reversible.
By monitoring symptoms, using regular blood tests, and following specialist guidance, tapering can be done safely.

You are not alone — your endocrine team will guide every step, especially if allergies (to prednisolone or hydrocortisone) make your case more complex.

With careful observation and a clear emergency plan, serious complications are rare and preventable.

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

🌿 Covid-19 and ABPA / Bronchiectasis: What Patients Need to Know

Many patients with ABPA, bronchiectasis, and asthma ask:

“If I test positive for Covid, am I at higher risk, and do I need antivirals or steroids?”
“Is Covid still a dangerous infection now that everyone has had it many times?”

Here’s what’s important right now.

🎯 Why you may be at higher risk

Having ABPA, bronchiectasis, or asthma doesn’t guarantee severe illness, but it does put you at higher risk compared to the average healthy adult. This means you are more likely to experience:

More severe Covid illness – infections can trigger worse chest symptoms (wheeze, shortness of breath, cough).
Secondary infections – bronchiectasis makes it easier for bacteria to grow in mucus after a viral infection.
Flares of existing disease – Covid can set off asthma attacks or ABPA flare-ups.
Slower recovery – fatigue, breathlessness, and extra sputum can last longer.

⚠️ Important: “Higher risk” does not mean you will definitely become very unwell. Many people with chronic lung disease still have mild Covid and recover fully at home.

✅ Current Covid treatments in the UK (2025)

Antivirals / monoclonal antibodies
- People with conditions like ABPA, bronchiectasis, or severe asthma may be eligible for medicines such as Paxlovid or Molnupiravir.
- These must usually be started within 5 days of symptoms or a positive test.
- Access is through the NHS Covid Medicines Delivery Unit (CMDU), often arranged via NHS 111 or your GP.
Steroids
- Oral steroids (prednisolone) are not routinely given for Covid unless oxygen levels drop, or you already take them for your lung condition.
- If your asthma/ABPA flares, follow your specialist’s guidance on when to start rescue steroids.
Antibiotics
- Covid is viral, so antibiotics don’t treat it directly.
- But if your doctor suspects a bacterial infection (e.g. in bronchiectasis), they may prescribe something like doxycycline.

🧾 Practical steps if you test positive

Call NHS 111 or your GP: Tell them you have ABPA/bronchiectasis/asthma and ask about referral for antivirals.
Monitor symptoms closely:
- Use a pulse oximeter if you have one (seek help if oxygen ≤94%).
- Watch for worsening breathlessness, chest pain, or confusion.
Keep safe at home: Ventilate rooms, use masks if possible, and wash hands often — though once exposed, focus mainly on monitoring and treatment.

🚨 When to seek urgent help

Severe shortness of breath
Oxygen levels ≤92–94%
Chest pain, confusion, or sudden collapse
→ Call 999

❓ Is Covid still dangerous in 2025?

Why it feels less dangerous now

Vaccination and immunity: Most people have had jabs and multiple infections, so later bouts are usually milder.
Variants: Current strains spread more easily but often cause less pneumonia than the original virus.
Better treatments: Antivirals and steroids (when needed) are widely available.

Why it can still be dangerous

Vulnerable groups: People with lung disease, weakened immunity, or older age are still more likely to need hospital care.
Exacerbations: Even mild Covid can set off asthma or ABPA flares, or worsen bronchiectasis infections.
Long Covid: Some people continue to develop fatigue, breathlessness, or brain fog lasting weeks to months.
Hospital admissions: Lower than during the pandemic, but NHS hospitals still see severe cases every winter.

👉 In summary: For most healthy people, Covid now feels like a bad cold or flu. For people with ABPA, bronchiectasis, or severe asthma, it can still be a dangerous infection — which is why monitoring and access to antivirals remain important.

✅ Key message

With ABPA and bronchiectasis, you are more vulnerable to complications from Covid. Most people still recover at home, but you may be eligible for antivirals. Steroids are only used if your underlying condition flares or if your oxygen drops. Stay alert, act quickly if symptoms worsen, and reach out for NHS support as soon as you test positive.

by GAtherton

When Antifungals Fail: One Patient’s Recovery from Subacute Invasive Aspergillosis After Surgery

Subacute Invasive Aspergillosis (SAIA) is a rare and serious lung infection caused by the Aspergillus fungus. It often affects people who are immunocompromised—whether due to illness or medications like immunosuppressants—and typically sits between chronic and acute invasive forms in severity.

🧬 A Patient's Story from Australia

“I was diagnosed with SAIA after being treated with immunosuppressants for an autoimmune condition. Over seven months, I tried three different antifungal medications—but the infection persisted. I was still producing thick mucus and felt systemically unwell, almost like I had a constant infection running through me.

Four weeks ago, I underwent a wedge resection—a type of surgery where the affected part of my lung was removed. Since then, my symptoms have completely resolved. I’m no longer coughing or feeling septic.

My infectious diseases specialist plans to keep me on posaconazole for 12 months, with monthly galactomannan blood tests to catch any recurrence early.

I’ve found there’s very little published about surgery for SAIA, so I hope my experience might help others.”

🧪 What Is SAIA?

SAIA is a slowly progressive lung infection that develops over weeks to months. Unlike acute invasive aspergillosis, which moves quickly, SAIA often occurs in people with some degree of immune suppression but who aren’t completely immunocompromised.
It can present with:

Persistent cough
Low-grade fever
Fatigue
Mucus production
Progressive lung damage

Standard treatment involves long-term antifungal therapy, often with drugs like:

Itraconazole
Voriconazole
Posaconazole

But in some cases—like this patient’s—antifungal therapy alone isn’t enough.

🛠️ When Is Surgery Used for SAIA?

Surgery, including wedge resection, may be considered when:

Antifungal medications are not effective
The infection is localized to one part of the lung
There is persistent or worsening lung damage
Patients are fit enough to undergo surgery

🔍 What Does the Evidence Say?

Although not commonly performed, surgery for aspergillosis is documented in medical literature, especially in cases of:

Chronic pulmonary aspergillosis (CPA)
Fungal nodules
Subacute forms like SAIA

Key studies:

A U.S. study of >100,000 aspergillosis cases found that only 4.8% underwent surgery, usually for treatment failure or severe complications.
A Chinese study of 85 CPA patients showed a relapse rate of only 7% post-surgery, with most patients improving dramatically.
A UK case series described 30 patients having lung resections over 15 years, showing surgery is safe and effective when performed in experienced centres.

🔄 What Happens After Surgery?

Even after a successful resection, follow-up antifungal treatment is often continued to prevent recurrence. Monitoring usually includes:

Regular imaging (CT scans)
Galactomannan blood tests (to detect fungal components)
Symptom tracking

This is typically guided by a multidisciplinary team involving infectious diseases, respiratory, and thoracic surgery specialists.

🎯 Key Takeaways

SAIA is uncommon, and when antifungals fail, surgery can be life-changing.
Wedge resection is a lung-sparing procedure that removes just the infected portion, offering good outcomes when the disease is localised.
Ongoing antifungal therapy and monitoring are critical to long-term success.
Your story adds to a growing but still limited body of knowledge and may help inform future treatment decisions and encourage further research.

If you are a patient or clinician navigating SAIA and struggling with antifungal treatment, this story may offer hope—and a reminder that surgical options, though rarely needed, can be effective when used judiciously.

by GAtherton

Other forms of aspergillosis: Aspergillus Empyema, A Rare and Serious Complication of Aspergillosis

What Is Aspergillus Empyema?

Aspergillus empyema is a very rare but serious fungal infection where Aspergillus invades the pleural space — the thin cavity between the lungs and the chest wall. Normally, this space contains a small amount of lubricating fluid. In empyema, it fills with infected pus, often due to rupture from a lung cavity or complication following severe illness or surgery.

In this form of aspergillosis, the infection goes beyond the lungs into the lining around the lungs (pleura), and is typically seen in people with severe underlying lung disease or who are very immunocompromised.

How Rare Is It?

Type of Aspergillosis	Estimated Cases per 100,000 People	How Common?	Who Is Most at Risk?
ABPA (Allergic Bronchopulmonary Aspergillosis)	~40–60	Moderately common	People with asthma or cystic fibrosis
CPA (Chronic Pulmonary Aspergillosis)	~3–4	Uncommon	People with underlying lung disease (e.g. TB, COPD)
Aspergilloma (fungus ball)	~0.5–1	Rare	People with lung cavities (often overlaps with CPA)
Aspergillus Empyema	< 0.1	Very rare	Severely immunocompromised or critically ill ICU patients

Most people living with ABPA or CPA will never develop Aspergillus empyema.

Who Is at Risk?

Risk of empyema increases in people who have:

Severely weakened immune systems (e.g. high-dose corticosteroids, cancer treatment, transplant)
Lung surgery, trauma, or chest drain procedures
A ruptured aspergilloma (fungus ball)
Existing lung cavities (from TB, sarcoidosis, or CPA)
Severe COVID-19 or ARDS (acute respiratory distress syndrome) with damaged lung tissue

Even among high-risk patients, Aspergillus empyema remains rare.

Symptoms

Fever that does not improve with antibiotics
Chest pain or tightness
Breathlessness
Cough (may be foul-smelling)
Persistent fluid seen on chest X-ray or CT scan

Diagnosis

Doctors may use:

CT scans or chest X-rays to detect fluid or cavities
Pleural fluid sampling (for fungal culture, galactomannan, PCR)
Tissue biopsy in difficult or unclear cases

Treatment Options

1. Drain the Infected Fluid

Chest drain (tube)
Surgical drainage in complex cases

2. Antifungal Therapy

Usually voriconazole (oral or IV)
Treatment may last months, depending on response

3. Surgery

May include decortication (removing infected pleura)
Repair of fistulas or ruptured cavities
Muscle or fat flaps to prevent recurrence and close space

4. Other Measures (used selectively)

Intrapleural antifungal instillation (amphotericin)
Endobronchial valves or spigots to manage air leaks

Outcomes and Prognosis

Historically high mortality (30–75%), mostly due to delayed diagnosis or underlying illness
Outcomes improving with specialist antifungal and surgical treatment
Early intervention saves lives

Summary for Patients

Aspergillus empyema is very rare, and affects only a tiny number of people with aspergillosis — usually those who are very unwell, immunocompromised, or post-surgery.
It is treatable with antifungals, drainage, and sometimes surgery.
Most people with ABPA or CPA will never experience this complication.
Stay aware of symptoms, and ensure regular check-ups if you have known lung cavities or risk factors.

by GAtherton