🌡️ Understanding Body Temperature in Aspergillosis: Why Your Fever May Look Different

Many people living with aspergillosis—including allergic bronchopulmonary aspergillosis (ABPA), chronic pulmonary aspergillosis (CPA), severe asthma with fungal sensitisation (SAFS) and Aspergillus bronchitis—notice that their body temperature behaves differently from what doctors call “normal.”

This is especially common in people who are:

  • On long-term steroids

  • Tapering steroids

  • Living with adrenal insufficiency

  • Older adults

  • On biologics

  • Managing chronic lung disease

This guide explains why your temperature may run lower, why fevers can appear smaller or absent, and how to safely manage this.


🔶 1. Many aspergillosis patients have a lower baseline temperature

Although “37.0°C” is often quoted, most patients actually sit anywhere between 35.5–36.5°C.
Reasons include:

✔ Long-term steroids

Prednisolone, methylprednisolone, hydrocortisone, and even high-dose inhaled steroids can blunt the immune response and lower your resting temperature.

✔ Adrenal insufficiency

If your adrenal glands are suppressed, your body’s ability to raise temperature is reduced.
You may get no fever at all, even with infections.

✔ Chronic lung disease

Living with ABPA, CPA or bronchiectasis can change how your body regulates heat.

✔ Biologic treatments

Some biologics influence inflammatory signalling and may soften fever responses.

✔ Age

Older adults naturally have:

  • Lower metabolism

  • Lower baseline temperature

  • Reduced ability to generate fever (“immune senescence”)

Many older aspergillosis patients sit around 35.7–36.2°C when completely well.


🔶 2. Fever is a rise from your normal — not a single number

For someone with a naturally low temperature, a fever may look very different.

A useful rule:

A fever = a rise of 1°C above your personal baseline,
even if the thermometer is below 38°C.

Example

  • Your baseline = 35.8°C

  • Your fever may begin at 36.8–37.0°C

You may feel shivery, hot, exhausted or “flu-ish” long before hitting 38°C.


🔶 3. Why fevers are often “muted” in aspergillosis

✔ Steroids

Reduce the body’s ability to trigger a strong fever.

✔ Adrenal insufficiency

Greatly reduces your ability to raise temperature; infections may show as fatigue, dizziness, nausea or sudden weakness instead.

✔ Age

Older adults may have:

  • No fever

  • A tiny rise

  • Confusion or breathlessness as the only sign of infection

✔ Chronic disease

Your temperature regulation system may simply behave differently because of long-term inflammation.


🔶 4. What YOU can do to manage this safely

Know your personal baseline

Measure your temperature twice daily for 5–7 days when well.
Record the average — this is your true normal.

Treat a 1°C rise as your own fever

Don’t wait for the thermometer to reach 38°C.

Watch symptoms more than the number

Seek medical advice if you notice:

  • Feeling feverish or shivery

  • Breathing worsening

  • New chest or flank pain

  • Sudden exhaustion

  • Increased heart rate

  • Confusion, dizziness or “not right”

  • New cough or change in sputum

These can indicate infection even without a high temperature.

Keep a symptom + temperature chart

Especially if you:

  • Are on steroids

  • Have adrenal insufficiency

  • Are tapering

  • Are on biologics

  • Have recurrent infections

Even simple notes help clinicians hugely.

Tell every clinician your temperature baseline

Not all doctors will know your usual pattern, so tell them:

“My normal temperature is around X°C.
I don’t get high fevers because of chronic illness/steroids/adrenal suppression.
A small rise is significant for me.”

This is important in GP appointments, A&E, respiratory clinics and hospital admissions.


🔶 5. Extra precautions if you have adrenal insufficiency

People with steroid-induced adrenal suppression must be especially careful:

  • A small temperature rise + feeling unwell may mean you need stress-dose steroids

  • Vomiting, dizziness, intense fatigue or confusion are warning signs

  • Always follow your adrenal emergency plan

  • Always carry your Steroid Emergency Card and hydrocortisone emergency injection if prescribed


🔶 6. Do doctors understand this?

Most clinicians understand the general rules:

  • Older adults often do not mount high fevers

  • Steroids blunt fever

  • Adrenal insufficiency changes the febrile response

  • Infection may present atypically

However, few clinicians know your personal baseline unless you tell them.

Sharing your own numbers helps them interpret your symptoms safely and accurately.


🟩 Summary for Aspergillosis Patients

  • Many people with aspergillosis have a naturally lower temperature.

  • Steroids, adrenal insufficiency and age can all reduce your ability to produce a fever.

  • A rise of 1°C above YOUR normal may be your fever.

  • Focus on overall symptoms, not just the thermometer.

  • Tell every clinician your baseline temperature.

  • Take extra care if you have adrenal insufficiency.


⭐ Recent Aspergillosis Research Updates (Week 48)

24 Nov 2025 — Collated new articles (curated highlights)

Top takeaways (clinician focus)

  • Burden & mortality: US death‑certificate analysis reinforces substantial aspergillosis‑attributable mortality; IA codes dominate—useful for advocacy and service planning (Walsh et al., CID 2025; PMID 41284728).
  • Diagnostics (CPA/ABPA & TB‑survivors): Senegalese post‑TB cohort preprint compares ELISA vs rapid serology for chronic Aspergillus infection—signals for programmatic screening but peer review pending (medRxiv PPR1125158).
  • Therapeutics & TDM: Multiple papers underscore voriconazole therapeutic drug monitoring nuances (beyond‑therapeutic levels; contribution of N‑oxide metabolite); anticipate practice pearls for ICU and complex cases.
  • Immunology & host‑directed therapy: IL‑37 review summarises antifungal‑modulating effects (↓NLRP3 signalling in murine aspergillosis). Casadevall editorial argues fungal vaccines are feasible (incl. aspirational protection for transplant recipients).
  • Comorbidity interfaces: Case data link ABPA with pleuro‑parenchymal Aspergillus infection; ECMO after heart transplant carries notable IA risk; A. niger conidia seen intracellularly in lung‑Tx cytology—diagnostic clue.
  • Antifungal susceptibility: Eastern India cohort provides local susceptibility mapping across ABPA/CPA/aspergilloma/IPA phenotypes—supports regional stewardship.
  • Policy/consensus: Asia Fungal Working Group Delphi consensus for mold pneumonia in resource‑limited settings—helpful for regional protocols.

Organised evidence table (with copy‑ready links)

  1. Aspergillosis‑attributable mortality (USA) — administrative/death‑certificate study
    Clin Infect Dis (2025) — Walsh TJ et al.
    PMID: 41284728
    https://pubmed.ncbi.nlm.nih.gov/41284728/
  2. Post‑TB cohort screening for chronic Aspergillus infection (ELISA vs RDT) — preprint
    medRxiv (2025) — Mariama T et al.
    PPR: PPR1125158
    https://www.medrxiv.org/ (search PPR1125158)
  3. Voriconazole TDM — beyond‑therapeutic levels in ICU IFI
    BMC Infect Dis (2025) — Lee YC et al.
    PMID: 41275081
    https://pubmed.ncbi.nlm.nih.gov/41275081/
  4. Voriconazole N‑oxide metabolite in TDM (case)
    Farm Hosp (2025) — Orozco Cifuentes I et al.
    PMID: 41274859
    https://pubmed.ncbi.nlm.nih.gov/41274859/
  5. Antifungal susceptibility of respiratory Aspergillus isolates (Eastern India)
    MicrobiologyOpen (2025) — Nikhil A et al.
    PMID: 41250899; PMCID: PMC12624224
    https://pubmed.ncbi.nlm.nih.gov/41250899/
    https://europepmc.org/article/PMC/12624224
  6. IL‑37 in respiratory disease (incl. aspergillosis models) — review
    Front Immunol (2025)
    PMCID: PMC12640846
    https://europepmc.org/article/PMC/12640846
  7. Fungal vaccines — feasibility editorial (aspergillosis included)
    J Clin Invest (2025) — Casadevall A
    PMID: 41243962; PMCID: PMC12618062
    https://pubmed.ncbi.nlm.nih.gov/41243962/
    https://europepmc.org/article/PMC/12618062
  8. Expert consensus: off‑label/novel antimicrobials (aspergillosis contexts cited)
    JAC Antimicrob Resist (2025)
    PMCID: PMC12641089
    https://europepmc.org/article/PMC/12641089
  9. ABPA with pleuro‑parenchymal aspergillus infection — case
    J Postgrad Med (2025) — Spalgais S et al.
    PMID: 41277380
    https://pubmed.ncbi.nlm.nih.gov/41277380/
  10. Aspergillus endophthalmitis post‑phaco — failed salvage — case
    Int Ophthalmol (2025) — Huang Z
    PMID: 41247646
    https://pubmed.ncbi.nlm.nih.gov/41247646/
  11. Heart Tx on ECMO — infections incl. IA — cohort
    Transplant Direct (2025) — Swiss Transplant Cohort
    PMID: 41268061; PMCID: PMC12629377
    https://pubmed.ncbi.nlm.nih.gov/41268061/
    https://europepmc.org/article/PMC/12629377
  12. Mold pneumonia in resource‑limited Asia — Delphi consensus
    Med Mycol (2025) — Asia Fungal Working Group
    PMID: 41251327
    https://pubmed.ncbi.nlm.nih.gov/41251327/
  13. A. niger conidia intracellular in AMs — lung Tx cytology clue — case
    Acta Microbiol Immunol Hung (2025)
    PMID: 41269231
    https://pubmed.ncbi.nlm.nih.gov/41269231/
  14. Out‑of‑pocket expenditure & QoL in CPA vs PTLD — comparative study
    J Infect Chemother (2025) — Titiyal R et al.
    PMID: 41274342
    https://pubmed.ncbi.nlm.nih.gov/41274342/
  15. Destroyed lung pneumonectomy — complications; CPA/haemoptysis associations
    J Surg Res (2025) — Yu L et al.
    PMID: 41270587
    https://pubmed.ncbi.nlm.nih.gov/41270587/
  16. Severe asthma immunity — activation signature independent of fungal sensitisation
    Mucosal Immunol (2025) — Plumpton EL et al.
    PMID: 41270906
    https://pubmed.ncbi.nlm.nih.gov/41270906/
  17. COVID‑19 & aspergillosis context — perspective linking co‑infection to chronicity risks
    Elife (2025) — Henrich TJ et al.
    PMID: 41247781; PMCID: PMC12622966
    https://pubmed.ncbi.nlm.nih.gov/41247781/
    https://europepmc.org/article/PMC/12622966
  18. NTM lung disease outcomes (Italian tertiary centre) — comorbidity context
    Sci Rep (2025) — Carli SM et al.
    PMID: 41249256; PMCID: PMC12623857
    https://pubmed.ncbi.nlm.nih.gov/41249256/
    https://europepmc.org/article/PMC/12623857
  19. Mixed mucor + IA coinfection in aplastic anaemia — fatal case
    J Med Case Rep (2025) — Javaherchian P et al.
    PMID: 41272805; PMCID: PMC12639702
    https://pubmed.ncbi.nlm.nih.gov/41272805/
    https://europepmc.org/article/PMC/12639702
  20. Sporotrichosis host genes; IA incidence observation — methods paper
    Sci Rep (2025) — Tang Z et al.
    PMID: 41272147; PMCID: PMC12638995
    https://pubmed.ncbi.nlm.nih.gov/41272147/
    https://europepmc.org/article/PMC/12638995
  21. SFTS complicated by IPA — prediction nomogram
    BMC Infect Dis (2025) — Yan R et al.
    PMID: 41275152
    https://pubmed.ncbi.nlm.nih.gov/41275152/
  22. Data resources landscape incl. Aspergillosis datasets — review
    J Med Syst (2025) — Pokutnaya D et al.
    PMID: 41273456; PMCID: PMC12640313
    https://pubmed.ncbi.nlm.nih.gov/41273456/
    https://europepmc.org/article/PMC/12640313
  23. Cell metabolism study using CAPA cohort as comparator
    Cell Mol Life Sci (2025) — Vasilogiannakopoulou T et al.
    PMID: 41258438; PMCID: PMC12630439
    https://pubmed.ncbi.nlm.nih.gov/41258438/
    https://europepmc.org/article/PMC/12630439
  24. Preprint: antibiotics → impaired neutrophil anti‑Aspergillus immunity (mouse)
    BioRxiv (2025) — Aufiero MA & Hohl TM
    PPR: PPR1122060
    https://www.biorxiv.org/ (search PPR1122060)
  25. Preprint: HosA HDAC in A. fumigatus virulence
    BioRxiv (2025) — Liu H et al.
    PPR: PPR1121973
    https://www.biorxiv.org/ (search PPR1121973)
  26. Pulmonary mucormycosis with necrotising pneumonia — differential includes aspergillosis
    BMC Pulm Med (2025) — Duong‑Minh N et al.
    PMID: 41254633; PMCID: PMC12625637
    https://pubmed.ncbi.nlm.nih.gov/41254633/
    https://europepmc.org/article/PMC/12625637
  27. Clove (S. aromaticum) essential oil in rabbit aspergillosis — preclinical
    Research Square (2025) — Shokrpoor S et al.
    PPR: PPR1121622
    https://www.researchsquare.com/ (search PPR1121622)
  28. Cross‑country multimodal evidence: Aspergillus & biliary atresia — hypothesis‑generating
    Gut Pathog (2025) — Huang SW et al.
    PMID: 41250124; PMCID: PMC12621361
    https://pubmed.ncbi.nlm.nih.gov/41250124/
    https://europepmc.org/article/PMC/12621361

🌿 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).


Side effects from Biologic Medication

It’s completely understandable to feel unsure before starting a biologic — especially when you’ve heard different experiences from different people.
Most patients with ABPA or severe Aspergillus-related asthma do very well on biologics. Side effects can happen, but they’re usually mild and settle quickly.

🌟 Most people report very few problems

Patients often say:

  • The injections are straightforward

  • They feel the same or better within days or weeks

  • There’s little or no impact on daily life

🌟 Common, mild side effects

These are the ones we hear most often across omalizumab, benralizumab, dupilumab and tezepelumab:

📌 Injection-site reactions

  • Redness

  • Itching

  • A small tender lump

  • Bruising
    These usually disappear within 24–48 hours.

📌 Mild tiredness

Some people feel slightly “wiped out” after the first few doses.

📌 Headache

Very common with the first injection. Less so afterwards.

📌 Minor joint or muscle aches

A bit like the feeling after a flu jab.

📌 Nasal or sinus changes

Occasional mild dryness or congestion, especially with dupilumab.

🌟 Less common (still mild)

  • Mild tummy upset

  • Sore throat

  • A brief “flu-ish” feeling

  • Temporary increase in eczema (mainly with dupilumab)

  • Slight mood dip for a day or two (rare)

🌟 Rare but important

These are very uncommon, and your team will explain what to look out for:

  • Allergic reaction shortly after an injection
    (This is why your first dose is supervised.)

  • Eye inflammation — mostly linked to dupilumab, usually mild and treatable

Your team will give you clear advice on what to do if anything unusual happens.

🌟 What ABPA patients often notice

People with ABPA frequently describe:
👉 Fewer allergic symptoms
👉 Clearer breathing
👉 Much less mucus
👉 Fewer flare-ups and fewer steroids

But biologics don’t help everyone — which is why the first few months are monitored closely.

🌟 Final reassurance

For many aspergillosis patients, biologics are far easier than long-term steroids or antifungals. Most say the benefits outweigh the side effects — but every person’s experience is individual.


**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):

  1. Higher doses can reduce more quickly.

  2. Taper slows dramatically near physiological levels
    (~4–6 mg pred-equivalent).

  3. If symptoms appear → pause, slightly increase, or slow taper.

  4. 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.


**Understanding Medicines in Rare Forms of Aspergillosis:

A Complete Guide for Patients with CPA, ABPA, SAFS and Aspergillus Bronchitis**

People living with chronic or allergic forms of aspergillosis often face treatments that fall outside the standard medicine licensing system. You may hear terms like off-label, unlicensed, specials medicines, or rare disease. This guide explains these concepts clearly and safely in a way that helps you feel informed and confident in your care.


⭐ 1. What is a rare disease?

In the UK and EU, a rare disease is defined as:

A condition affecting fewer than 1 in 2,000 people
(≈ fewer than ~33,500 people in the UK)

Although each rare disease affects relatively few people, over 7,000 rare diseases exist, so collectively they affect 1 in 17 people.


⭐ 2. Are CPA, ABPA, SAFS and Aspergillus Bronchitis rare diseases?

Here is how the main Aspergillus-related conditions compare to the rare-disease definition.

Chronic Pulmonary Aspergillosis (CPA)

  • ~3,600 diagnosed UK patients (under-diagnosis likely, but still rare).
    CPA is officially recognised as a rare disease.


Allergic Bronchopulmonary Aspergillosis (ABPA)

  • Occurs in 2.5–5% of all people with asthma.

  • UK estimate: 125,000–250,000 patients.
    ABPA is NOT a rare disease (but it is under-recognised).


Severe Asthma with Fungal Sensitisation (SAFS)

  • ~8,000 estimated UK cases.
    SAFS meets the definition of a rare disease.


Aspergillus Bronchitis

  • Likely <10,000 UK patients.
    Aspergillus Bronchitis qualifies as a rare disease.


Summary Table

Condition Approx UK Patients Rare Disease?
CPA ~3,600 ✔ YES
ABPA 125,000–250,000 ✘ NO
SAFS ~8,000 ✔ YES
Aspergillus Bronchitis <10,000 ✔ YES

Understanding whether a condition is rare helps explain why some treatments fall outside standard licensing.


⭐ 3. What is “off-label” prescribing?

Every medicine has a licence describing:

  • the condition it treats

  • dose

  • age group

  • how long it can be used

  • route (tablet, injection, inhaler)

Off-label means a doctor uses a licensed medicine in a way not included in the licence.

This can mean:

  • different disease

  • different dose

  • different age group

  • different route

  • different duration

Off-label prescribing is safe, legal, common and essential, especially in rare diseases.


⭐ 4. What is an “unlicensed” medicine?

An unlicensed medicine is one that has no UK licence at all.

Examples:

  • a medicine made specially for one patient (“specials”)

  • a liquid formulation when only tablets are sold

  • imported medicines licensed in another country

  • alternatives for patients with drug allergies

Unlicensed does not mean unsafe — it means the medicine isn’t commercially licensed in the UK.


⭐ 5. Why are off-label and unlicensed medicines common in rare diseases?

Rare diseases like CPA, SAFS and Aspergillus bronchitis:

  • affect small patient numbers

  • often have no licensed treatment

  • rely on specialist expertise and experience

  • require individualised dosing

  • cannot wait for slow or expensive licensing processes

Without off-label and unlicensed medicines, many rare-disease patients would have no treatment options.

This is why specialist centres exist.


⭐ 6. Biologics for ABPA: NOT licensed, but safe and widely used

This is a key point for patients.

No biologic is licensed for ABPA

(as of 2025)

Not licensed for ABPA:

  • Omalizumab (Xolair)

  • Mepolizumab (Nucala)

  • Benralizumab (Fasenra)

  • Dupilumab (Dupixent)

All biologics used in ABPA are therefore off-label.

⭐ Why do specialists use them anyway?

Because evidence is strong that biologics:

  • reduce ABPA flare-ups

  • reduce steroid need

  • improve lung function

  • improve symptoms

  • control eosinophilic/IgE-driven inflammation

  • reduce hospital admissions

ABPA lacks a commercially licensed biologic
→ but specialist evidence supports them strongly.

This is high-quality off-label prescribing.


⭐ 7. How do doctors decide what evidence is “good enough”?

Doctors use several acceptable forms of evidence, including:

✔ Randomised controlled trials

✔ National/international guidelines

✔ NAC / BTS / ECCMID / IDSA specialist protocols

✔ Observational studies and real-world evidence

✔ Case series and case reports

✔ Pharmacological reasoning (mechanisms of disease)

✔ MDT (multidisciplinary team) agreement

✔ Expert clinical experience (important in rare diseases)

All of these count as legitimate evidence.

Rare-disease medicine relies on the best available evidence, not only the “highest-level” evidence.


⭐ 8. Who holds responsibility if something goes wrong?

The prescriber carries responsibility, even for:

  • off-label use

  • unlicensed medicines

  • imported medicines

  • specials items

They must:

  • justify the decision

  • explain risks and benefits

  • obtain consent

  • document

  • monitor

If they follow guidance, they are fully protected by:

  • NHS indemnity

  • GMC standards

  • Trust governance

Patients are not responsible for adverse outcomes.


⭐ 9. Is this risky for the doctor?

Only if done unsafely.

When the doctor:

✔ follows specialist guidelines
✔ explains the situation
✔ documents their reasoning
✔ uses MDT support
✔ monitors closely

…the risk is minimal and fully protected.

In rare diseases, NOT prescribing off-label can be riskier if it denies a patient effective treatment.


⭐ 10. How are patients protected?

Patients with CPA, ABPA, SAFS or Aspergillus bronchitis are protected by:

  • careful MDT assessment

  • specialist supervision

  • decades of centre experience

  • guideline-supported decisions

  • regular reviews and monitoring

  • clear communication and consent

  • NHS governance systems

Your care is safe, structured and evidence-based.


⭐ Final reassurance for Aspergillosis patients

If you have CPA, ABPA, SAFS or Aspergillus bronchitis:

  • You are not receiving “experimental” treatment.

  • Off-label or unlicensed medicines are normal, safe, and essential.

  • Your specialist team carries the responsibility for these decisions.

  • Biologics for ABPA are off-label because licensing is slow — not because they are untested.

  • You are protected by national standards, MDTs, and specialist expertise.

  • Your treatment is based on the best available evidence, even when the condition is rare.

This is expert, modern care designed to give you the best possible outcome.


🌿 Your Immune System, Biologics, and Steroids: What’s Suppressed — and What Stays Strong

A clear, reassuring guide for people living with ABPA, CPA, asthma, SAFS, or bronchiectasis

Treatments for aspergillosis-related conditions often involve steroids, and more recently, biologics.
Many patients understandably wonder:

  • What do these medicines suppress?

  • Do they affect my ability to fight infection?

  • Why are biologics considered safer than long-term steroids?

  • Which parts of my immune system stay strong?

This guide explains the full picture in simple terms.


🧬 1. Understanding Your Immune System: The Three Layers

Your immune system has three major lines of defence.


A. Barriers — the first line

These stop pathogens entering in the first place:

  • Skin

  • Mucus in airways

  • Cilia sweeping mucus out

  • Tears, saliva, stomach acid

  • Healthy bacteria (microbiome)

👉 Biologics do NOT affect barriers.
👉 Steroids can weaken skin and airway lining if used long-term.


B. Innate immunity — fast responders

These act within minutes or hours.

Key cells:

  • Neutrophils → main killers of Aspergillus

  • Macrophages → engulf spores

  • Dendritic cells → show pathogens to T-cells

  • NK cells → kill virus-infected cells

Sensors:

  • Dectin-1 → recognises fungal walls

  • TLRs

  • Complement proteins

👉 Biologics do NOT weaken these.
👉 Steroids weaken several key functions, especially neutrophils and macrophages.


C. Adaptive immunity — targeted, long-term defence

Slower but specialised.

T-cells:

  • Th1 → fight bacteria/viruses

  • Th17 → major antifungal fighters

  • Th2 → allergic pathways (IgE, eosinophils)

  • Tregs → calm inflammation

B-cells & antibodies:

  • IgG / IgA / IgM → normal infection defence

  • IgE → allergy and ABPA pathway

👉 Biologics only suppress Th2/IgE pathways.
👉 Steroids suppress many T-cell and B-cell functions, not just allergy.


🎯 2. What Biologics Suppress (Targeted & Selective)

Biologics used in ABPA and difficult asthma (omalizumab, mepolizumab, benralizumab, dupilumab, tezepelumab) only turn down allergic inflammation, not infection-fighting immunity.

🔻 A. They suppress:

  • IgE

  • Eosinophils

  • IL-4 / IL-5 / IL-13

  • Type-2 allergic inflammation

  • Mucus hypersecretion (IL-13)

  • TSLP airway alarm signalling

🛡️ B. They do NOT suppress:

  • Neutrophils

  • Macrophages

  • Th1 immunity

  • Th17 antifungal pathways

  • T-cell killing function

  • Antibiotic/cell-mediated defences

  • Complement

  • Dectin-1 fungal recognition

This is why biologics do NOT increase fungal infection risk.


🔥 3. What Oral Steroids Suppress (Broad & Non-Specific)

Oral steroids like prednisolone reduce inflammation everywhere — including places you need for infection defence.

A. They suppress key immune cells

  • Neutrophils → move slower, kill less effectively

  • Macrophages → reduced pathogen killing

  • T-cells → weaker antiviral/antifungal defence

  • B-cells → reduced antibody production

B. They suppress important cytokines

  • IL-1, IL-2, IL-6

  • TNF-α

  • Interferons

  • IL-12, IL-23 (Th1/Th17 pathways)

These are essential for fighting viruses, bacteria, and fungi.

C. They weaken antigen presentation

Dendritic cells and macrophages become less effective at “showing” pathogens to T-cells.

D. They weaken barriers

  • Thinner skin

  • Thinner airway lining

  • Slower wound healing

This increases infection risk.

E. They reduce eosinophils and IgE (similar to biologics)

But they do this alongside suppressing many healthy parts of your immune system.


🛡️ 4. What Remains Intact on Each Treatment

✔ On biologics (strongest preserved immunity):

  • Neutrophil antifungal killing

  • Macrophage function

  • Th1 & Th17 immunity

  • Antibodies (IgG, IgA, IgM)

  • Complement

  • Mucus & cilia defences

  • NK cell antiviral defence

  • Fever & inflammation responses

⚠️ On steroids (weaker preserved immunity):

  • Complement

  • Some antibody production

  • Basic barrier function (though thinner)

Many infection-fighting cells work less effectively.


🫁 5. Why Biologics Are Safer Long-Term for ABPA/SAFS

Because biologics:

  • target only a tiny portion of immunity

  • do not increase fungal growth

  • do not raise infection risk

  • reduce inflammation without broad suppression

  • help avoid long-term steroid complications

Steroids:

  • increase infection risk

  • can worsen fungal colonisation

  • damage lung structure over time

  • cause weight gain, bone thinning, adrenal issues

  • must be used short-term only when essential


🌈 6. Summary Table

Immune Feature Biologics Steroids
IgE suppression
Eosinophil suppression
Neutrophils Unaffected Suppressed
Macrophages Unaffected Suppressed
Th1/Th17 antifungal pathways Unaffected Suppressed
Viral defence Unaffected Suppressed
Barrier integrity Unaffected Weakened
Infection risk No increase Increased
Long-term safety High Low

🌟 7. One-Sentence Takeaway

Biologics turn down the allergic part of immunity (IgE, IL-4, IL-5, IL-13, eosinophils), while steroids suppress many of the infection-fighting parts as well — which is why biologics are much safer long-term.


🌿 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.


⭐ How to Avoid Being Fooled by Misleading Products, Private Tests and Health Claims

A practical, evidence-based guide for people living with aspergillosis, asthma, bronchiectasis and COPD

People with long-term lung conditions are often targeted by persuasive marketing, “health influencers”, alternative practitioners, and private test companies.
These services frequently exploit fear, frustration, and the very understandable desire for answers.

This expanded guide explains why certain products look scientific, why most are biologically impossible, and how you can protect yourself from being misled or spending money on things that cannot help your condition.

This is about empowerment — never about blaming patients.


🧩 1. Why misleading products look convincing

Companies deliberately use wording and imagery that trigger trust:

  • lab coats

  • microscopes

  • graphs and biological diagrams

  • words like “antifungal”, “immune”, “toxins”, “wellness”, “clinical strength”

These features make a product appear evidence-based — but appearance is not evidence.

Many claims contain a grain of truth, e.g.:

  • “Tea tree oil kills fungus in the lab”

  • “Silver has antimicrobial properties”

  • “This herbal extract reduces inflammation in laboratory tests”

But the missing information is the critical part:

⭐ The lab conditions have nothing to do with the human body.

To “kill fungus in a dish”, companies use concentrations that:

  • would be toxic in humans

  • cannot reach the lung tissue

  • would be broken down in the gut or bloodstream

  • do not survive into the airways

Companies rely on the fact that most customers don’t know this.


🧬 2. “Plausibility comes before testing” — the rule companies hope you don’t know

Scientists follow a simple chain:

1️⃣ Is it plausible?
Can the substance reach the lung?
Does the pathway make sense?

2️⃣ If yes — test it.
If not — don’t.

Products sold online almost always fail at Step 1.

Examples:

Turmeric supplements

Even at huge oral doses, only a tiny amount enters the bloodstream — nowhere near the lung in meaningful levels.

Oregano oil

Kills fungi on metal plates in labs — but the amount needed inside the lung would be toxic.

Silver products

Irritate the lungs and accumulate in tissues — highly implausible as therapy.

Essential oils

Break down long before reaching the airways in meaningful amounts.

Herbal antifungals

Often metabolised by the gut and liver — never reach airways at therapeutic levels.

This is why clinical trials don’t happen —
not because no one has tried,
but because there’s no scientific reason to bother.


🛍️ 3. How companies use “allowed” claims to sound medical

Because these products are not classed as medicines, they must not claim to “treat disease”.
So companies use vague, legally safe wording:

  • “Supports immunity”

  • “Maintains wellness”

  • “Promotes respiratory health”

  • “Contains antifungal botanicals”

  • “Helps with mould exposure”

  • “Advanced detox science”

All of these sound medical but say nothing measurable.

Example:

A supplement cannot say:

  • “Improves aspergillosis symptoms”

But it can say:

  • “Supports healthy immune response”

This tricks the viewer into mentally connecting the dots without the company making any illegal claims.


🧊 4. Air filters — the rare partial exception

Air purifiers can help some people, because they reduce:

  • dust

  • pollen

  • irritants

  • pet dander

  • airborne particulate matter

These changes may ease coughing or wheezing in sensitive people.

BUT…

most devices sold online are far too weak.

A purifier needs:

  • True HEPA H13 filter (not “HEPA-type”)

  • CADR 250–350+ for most rooms

  • Strong fan to turn over room air 4–5 times per hour

Without these, a purifier is just an expensive fan.

What they cannot do:

  • cure aspergillosis

  • remove Aspergillus from the lungs

  • prevent exposure

  • substitute for ventilation

  • fix damp or mould in walls

They improve comfort, not disease.


👩‍⚕️ 5. Why alternative practitioners are so persuasive

Alternative practitioners often:

  • speak with confidence

  • promise personalised care

  • provide long consultations

  • listen sympathetically

  • use scientific-sounding language

  • offer simple explanations for complex symptoms

Their tests and treatments look legitimate, but the problems include:

❌ No training in lung disease

❌ Misunderstanding of immunology

❌ Misuse of lab dish studies

❌ Incorrect interpretation of “toxins”

❌ Selling supplements with no evidence

❌ Recommending dangerous inhaled substances (e.g., oils, peroxide)

❌ Relying on anecdotes, not data

Even well-meaning practitioners can unintentionally cause:

  • lung irritation

  • drug interactions

  • adrenal effects

  • delays in proper NHS treatment

  • unnecessary fear


🧪 6. Private test companies — why their results look real but mean nothing

Common private tests include:

  • mycotoxin urine tests

  • “mould illness panels”

  • detox pathway testing

  • food IgG tests

  • fungal metabolite tests

  • heavy metal hair analysis

  • “immune balance” panels

  • testosterone finger-prick kits

These results are presented with:

  • charts

  • colour-coded ranges

  • expert-sounding commentary

But the key issue is:

⭐ The reference ranges are invented by the company.

Often “high” simply means:

  • “higher than the average of people who bought this test”

Not:

  • higher than healthy people

  • higher than unwell people

  • linked to disease

GPs and consultants cannot act on these results because they are not medically interpretable.


👨‍⚕️ 7. Testosterone tests — a perfect illustration of misleading health screening

Companies advertise:

  • “Tired? Low mood? Low motivation?”

  • “Check your testosterone at home”

  • “Feel younger again”

They use US-style messaging that implies easy treatment.

But in the UK, testosterone treatment requires:

  • symptoms consistent with hypogonadism

  • two morning venous blood tests

  • validated hospital labs

  • endocrine specialist interpretation

  • ruling out multiple other causes

  • testosterone levels fall slowly as part of ageing - it is normal

Finger-prick tests do not meet NHS criteria,
so patients end up:

  • anxious

  • misinformed

  • sold supplements

  • not eligible for NHS treatment

This perfectly mirrors the broader pattern of private testing.


🔍 8. The “curiosity gap”: why people buy tests that GPs won’t order

Patients understandably feel:

  • frustrated

  • curious

  • confused

  • not listened to

  • desperate for answers

When a GP says “That test won’t help,” it can feel like:

  • rejection

  • dismissal

  • obstruction

But the reality is:

⭐ GPs are following evidence-based pathways to protect you.

Most private tests:

  • do not answer a clinical question

  • have false positives

  • trigger unnecessary follow-up scans

  • cause anxiety

  • cannot be interpreted

  • do not influence treatment

Private companies exploit:

  • curiosity

  • frustration

  • the desire for answers

  • the emotional gap left by long waits or unexplained symptoms

But a meaningless test result is worse than no test at all.


🧾 9. Real-world examples: 15 common traps to avoid

1. Mould settle plates

All rooms grow mould on plates — totally meaningless for health.

2. IgG food sensitivity tests

Measure normal immune exposure, not allergies.

3. Finger-prick vitamin tests

Often inaccurate and label normal levels as “borderline”.

4. Lung detox drinks

Nothing you drink detoxes the lungs.

5. Hydrogen peroxide / silver nebulisers

Dangerous. Irritate lungs. Risk chemical burns and pneumonitis.

6. Essential oil diffusers marketed as “antifungal”

Irritate airways; no delivery to lung tissue.

7. Mycotoxin detox programmes

Based on non-diagnoses; push expensive supplements.

8. Immune-boosting products

No supplement boosts immunity in a useful way for aspergillosis.

9. “Black mould blood tests”

No such test exists; ranges are invented.

10. Ozone machines and air ionisers

Harmful to lungs; zero evidence.

11. Anti-mould paint additives

Mask damp; do not impact indoor fungal counts long term.

12. Red-light therapy devices

Cannot penetrate tissue; no lung benefit.

13. Detox foot patches

Turn brown from sweat; total scam.

14. Anti-mould laundry boosters

Irrelevant to aspergillus exposure.

15. Humidifiers sold for “lung support”

Raise humidity → increase mould risk.


🛡️ 10. The Anti-Fooling Checklist

Before you buy anything, ask:

✔ Has this been tested in people with aspergillosis?

✔ Can it physically reach the lungs?

✔ Does NHS medicine recognise or use it?

✔ Are the claims vague? (“supports immunity”)

✔ Are the reference ranges medically valid?

✔ Would my consultant recommend this?

✔ Is this a simple answer to a complex condition?

If any answer is no, it’s a red flag.


11. Golden rule

If a treatment or test genuinely helped aspergillosis, your consultant would already be using it —
not influencers, Amazon sellers, or unregulated US labs.


🌟 12. Final message: It’s not foolishness — it’s human

You are not being “tricked” because you’re naïve.
These products are engineered to be emotionally irresistible.
People with chronic illness are targeted because they are thoughtful, curious, and trying hard to get better.

If you are ever unsure about a product or test:

  • ask NAC/CARES

  • ask your specialist

  • or bring it to your next appointment

You deserve real answers — not false hope.


ECFG 2025: Key Aspergillus and Antifungal Insights for Patients and Clinicians

The European Conference on Fungal Genetics (ECFG 2025) gathered the leading fungal biology teams from across the world. Although primarily a genetics meeting, several abstracts offered direct clinical relevance for people living with aspergillosis or those working in the field.

The research covered here focuses on:

  • Aspergillus fumigatus

  • mechanisms of disease

  • resistance to antifungals

  • emerging antifungal treatments

  • environmental drivers of disease

  • insights relevant to CPA, ABPA, SAFS, bronchiectasis and invasive aspergillosis


Summary of Key Themes

1. Aspergillus genetic diversity is much greater than assumed

Pangenome work showed A. fumigatus strains possess different virulence genes and resistance traits. This may explain differences in how patients respond to infection and medication.

2. Environmental azole resistance continues to rise

Multiple abstracts confirmed that resistant strips often originate outdoors, shaped by climate, fungicides, soil chemistry, and climate change.

3. Promising new antifungals are advancing

Manogepix shows excellent activity against resistant strains, while several early-stage compounds (such as G-quadruplex ligands) represent brand-new modes of action.

4. Insights into virulence, persistence and treatment failure

Studies on hyphal fusion, echinocandin tolerance, and hypoxia adaptation shed light on chronic and resistant infections.

5. Improved tools accelerate antifungal discovery

CRISPR and genus-wide sequencing speed up the search for new drug targets and better diagnostics.


ECFG 2025 — Table of All Aspergillus / Aspergillosis / Antifungal-Relevant Abstracts

ID Title Lead Author / Presenter Institution Category Why It Matters
WS1.19 Reference pangenomes for A. fumigatus Marion Perrier Friedrich Schiller University, Jena Genomics / Evolution Reveals hidden genetic diversity linked to virulence and resistance.
WS1.20 Antifungal modes of action of G-quadruplex ligands Isabelle Storer University of East Anglia New antifungal mechanisms Suggests a brand-new antifungal class targeting fungal DNA structures.
WP1.2 NL1 as anti-virulence compound Jorge Amich ISCIII, Spain Virulence / Therapeutics May reduce disease severity without relying on killing the fungus.
WP1.6 Ace2 and RAM pathway regulation Devi N. J. Bale Pathogenesis Controls tissue invasion, morphology and possibly drug sensitivity.
WP1.8 Hyphal fusion and multi-drug resistant heterokaryons Michael Bottery University of Manchester Resistance mechanisms Shows resistance traits may spread between strains via fusion.
WP1.10 Manogepix activity against A. fumigatus Sean Brazil Trinity College Dublin New antifungals Strong activity including against resistant strains and biofilms.
WP1.14 ZfpA and echinocandin tolerance Dante Calise University of Wisconsin Echinocandin tolerance Explains how fungi sometimes survive caspofungin and related drugs.
WP1.16 Genetic background of azole-resistant A. fumigatus Saioa Cendón-Sánchez University of the Basque Country Environmental resistance Confirms resistant genotypes circulate between the environment and patients.
WP1.18 Genus-wide sequencing of Aspergillus Ronald P. de Vries Westerdijk Institute Evolution / Pathogenicity Identifies traits making some species pathogenic to humans.
WP1.22 Climate, soil & fungicide impacts on Aspergillus Thomas Easter University of Manchester Environmental epidemiology Links climate change and fungicides to rising azole resistance.
WP1.32 Multiplex CRISPR to accelerate antifungal research Fabio Gsaller Research tools Speeds identification of resistance pathways and drug targets.
WP1.42 Hypoxia-driven adaptations in A. fumigatus Olaf Kniemeyer Pathogenesis Explains persistence of A. fumigatus in low-oxygen lung cavities (CPA).

Detailed Clinical Relevance of the Findings

1. Rising environmental resistance

Azole-resistant A. fumigatus continues to emerge in agricultural and urban settings. Resistant spores are carried in air and soil, meaning people inhale them in daily life. This is especially relevant to those with CPA, ABPA, bronchiectasis and immunosuppression, who are more vulnerable.

Why it matters:
Resistant strains are a growing cause of treatment failure.


2. New antifungal treatments are progressing

Manogepix shows potent activity against resistant Aspergillus and biofilms, key in difficult-to-treat CPA and invasive aspergillosis.

G-quadruplex ligands and NL1 represent early steps toward new antifungal classes, extremely important after two decades of limited drug options.


3. Virulence and survival mechanisms explain persistent disease

Hypoxia adaptation (low-oxygen survival) helps explain why Aspergillus persists in lung cavities.
Hyphal fusion may allow rapid spread of resistance traits.
Echinocandin tolerance mechanisms (ZfpA) reveal why some invasive cases fail to respond.

Why it matters:
These insights help clinicians anticipate treatment difficulties and inform research for new therapies.


4. Better genomic tools support faster discovery

Multiplex CRISPR and pangenomic databases allow scientists to uncover gene functions much faster. This shortens the path to new antifungal development and improves understanding of how resistance evolves.


Conclusion

ECFG 2025 provides important clues about why Aspergillus disease is so persistent, why azole resistance is increasing, and how new antifungal drugs may overcome today’s challenges. It also reinforces that environmental drivers — including fungicide use and climate factors — are a major part of the problem.

For patients, clinicians, and researchers, these findings highlight a rapidly evolving landscape in aspergillosis research, with promising signs of future treatment improvements.