Why do some people with aspergillosis lose weight on the hips and thighs, but gain around the waist?

Many people living with aspergillosis, bronchiectasis or ABPA notice their body shape changing as they get older — especially after 60.
A very common pattern is:

Thinner hips and legs
More weight around the waist or tummy

This can feel confusing, but there are clear reasons why it happens.

1. Chronic lung conditions make it harder to keep leg and hip muscle

When you live with a long-term lung condition, you often have:

Breathlessness
Fatigue
Repeated chest infections
Less ability to walk long distances or climb stairs

Because the legs work harder than any other muscles, they are the first to lose strength and size when activity drops.
This is why many people notice:

Slimmer thighs
Smaller hips
Feeling weaker when getting out of a chair

This is partly due to age, but it happens faster in people with chronic lung disease.

2. Steroids can move weight from the limbs to the waist

Many aspergillosis patients have had:

Several courses of prednisolone over the years
High-dose inhaled steroids
Hydrocortisone replacement for adrenal problems

Even short or occasional courses can cause fat redistribution, where:

Fat and muscle reduce in the arms, hips and legs
More fat settles around the stomach area
The centre of the body becomes rounder even if the overall weight hasn’t changed much

This effect can continue long after stopping steroids.

3. Ageing naturally shifts fat towards the waist

After about age 60, the body changes how it stores fat:

Less around the hips and thighs
More around the waist
More “internal” fat around organs (visceral fat)

This happens to everyone, but can be more noticeable in people with aspergillosis because illness already reduces leg muscle.

4. You can lose muscle even if weight on the scales stays the same

Many patients say,
“I feel thinner and thicker at the same time.”

That’s because:

Muscle in the legs may be lost
Fat around the waist may increase
The total body weight doesn’t always change much

This is a normal pattern in long-term lung disease.

5. Illness, flare-ups, infections and poor appetite add to this

During flare-ups or infections, it’s common to:

Eat less
Feel exhausted
Lose muscle faster
Keep or gain tummy fat

The body burns muscle first when unwell, not fat — especially not tummy fat.

Is this dangerous?

Not usually on its own — but it does mean:

Legs may feel weaker
Balance and stamina can reduce
It may be harder to stay active

Strength and gentle exercise (within your limits) can help rebuild some leg muscle.

If weight changes are sudden or unexplained, they should always be discussed with your GP or specialist.

In summary

This body-shape change is very common in people with aspergillosis over 60.
It’s caused by a combination of:

Reduced activity due to breathlessness
Loss of leg and hip muscle
Steroid effects on fat distribution
Natural age-related changes
Appetite changes during illness

It doesn’t mean you’re doing anything wrong — it’s simply a pattern seen in many people with long-term lung disease.

by GAtherton

Physiotherapy and Aspergillosis: Why It Matters

Physiotherapy is an important part of care for many people with aspergillosis, including allergic bronchopulmonary aspergillosis (ABPA), chronic pulmonary aspergillosis (CPA), aspergillus bronchitis, and severe asthma with fungal sensitisation (SAFS).
It doesn’t diagnose the disease on its own, but physiotherapists play a key role in detecting symptoms, collecting good sputum samples, and helping patients stay stable.

1. How Physiotherapy Helps With Diagnosis

🔍 A. Spotting patterns of sputum, breathlessness, and airway clearance problems

Respiratory physiotherapists often notice:

Thick, sticky mucus that is difficult to clear
Recurrent phlegm plugs
Wheeze, crackles, or airflow changes
Reduced ability to clear secretions after infection
These patterns can be early clues pointing toward ABPA, aspergillus bronchitis, or bronchiectasis linked to Aspergillus.

🔍 B. Supporting high-quality sputum collection

A good sputum sample is essential for:

Fungal culture
PCR
Galactomannan tests
Antibiotic/antifungal susceptibility testing

Techniques like huff coughing, breathing control, postural drainage, or using devices such as Acapella or Aerobika help ensure the sample comes from deep in the lungs, not just saliva.

🔍 C. Identifying airway collapsibility or dysfunctional breathing

Physiotherapists can pick up:

Tracheobronchomalacia
Inducible laryngeal obstruction
Breathing pattern disorder
These are often overlooked and can mimic or worsen aspergillosis symptoms.

If a physio notices these features, they feed findings back to the medical team, supporting a faster, more accurate diagnosis.

2. How Physiotherapy Helps With Treatment

🫁 A. Airway clearance

One of the biggest challenges in aspergillosis—especially ABPA, CPA, and bronchiectasis—is mucus.
Physiotherapy helps patients learn techniques to keep the lungs clear:

Active Cycle of Breathing Techniques (ACBT)
Huffing
Directed huff / forced expiration technique
Gravity-assisted drainage
Oscillating PEP devices (Acapella/Aerobika)
Autogenic drainage
Saline nebulisers to thin mucus

Keeping the airways clear:

Reduces cough and breathlessness
Helps antifungal treatment reach affected areas
Lowers risk of infection and flare-ups
Improves quality of life

💨 B. Managing breathlessness and fatigue

Physiotherapists teach:

Breathing control
Pacing techniques
Positions of ease
Diaphragmatic breathing
Inspiratory muscle training (if appropriate)

This is especially valuable for patients with:

ABPA flare-ups
CPA with reduced lung capacity
COPD or asthma overlap
Deconditioning after illness

🏃 C. Exercise, strength, and rehabilitation

Long-term aspergillosis can reduce fitness due to:

Repeated infections
Inflammation
Steroid side-effects
Time spent resting

Physios provide personalised rehab plans to rebuild:

Strength
Endurance
Balance
Activity levels
Confidence

🧠 D. Managing the “vicious cycle” of breathlessness and anxiety

Breathlessness naturally triggers anxiety, which then worsens breathlessness.
Physiotherapists help break this cycle through:

Breathing retraining
Relaxation strategies
Education on pacing and control

This also reduces the number of A&E visits for “flare-ups” that are actually driven by breathlessness-anxiety spirals.

3. Supporting Long-Term Stability

Regular physiotherapy follow-up helps patients:

Spot flare-ups early
Adjust airway clearance routines
Stay active despite chronic illness
Prevent hospital admissions
Maintain independence

For many patients with aspergillosis, physio becomes a key part of long-term disease management, just like antifungals, inhalers, and specialist review.

4. When Should Patients See a Physiotherapist?

Physiotherapy is particularly helpful if you have:

ABPA with repeated mucus plugging
CPA with sputum, breathlessness, or reduced activity
Bronchiectasis
Frequent chest infections
Difficulty producing sputum for testing
Breathing pattern disorder
Muscle weakness from steroids or long illness
Unexplained breathlessness
Tracheal or airway collapsibility

Summary

Physiotherapy is not just an “add-on” to aspergillosis care—it is a core part of both diagnosis and treatment.
Physiotherapists help:

Identify airway issues
Support accurate testing
Improve breathing control
Clear mucus
Build strength and stamina
Stabilise long-term disease

This combination leads to better outcomes, fewer infections, and a better quality of life.

by GAtherton

⭐ Key Themes This Week (weekly updates Early December 2025: week 49)

1. CPA as an Immune Dysfunction Syndrome – Not Just Structural Lung Disease

Two papers (Janssen et al., Aegerter et al.) add weight to the concept that chronic pulmonary aspergillosis (CPA) is driven not only by underlying lung architecture but by defects in host immunity, including:

Impaired IFN-γ production
Inflammatory effects of Charcot–Leyden crystals (CLC) in mucus
These findings support future directions in host-directed therapy and targeted immunological profiling.

2. Improved Diagnostics: Molecular, Imaging & Bronchoscopy

Significant focus this week on diagnostic innovation:

PCR and multi-target molecular testing in cancer patients (Rickerts et al.)
Radiolabelled siderophore imaging capable of identifying infected regions early (Dvorakova Bendova et al.)
Bronchoscopic signatures of tracheobronchial aspergillosis (Tapia Barredo et al.)
Together, these highlight a shift toward rapid, non-invasive, high-sensitivity diagnostics for invasive and chronic disease.

3. Global Variation in Antifungal Resistance

The Indian susceptibility study (Nikhil et al.) reinforces the strong geographic variability in Aspergillus susceptibility patterns. This may influence both local empiric practice and global surveillance needs.

4. Increasing Recognition of ABPA Beyond Classic Asthma

ABPA continues to be diagnosed in wider groups, including asthma–COPD overlap (Wang et al.), eosinophilic diseases, and cases overlapping with autoimmune conditions (Chakravarty et al.).
This implies:

A need for broader screening,
Awareness that ABPA can mimic inflammatory or autoimmune disease.

5. High ICU Burden – Viral/Fungal Interactions Persist

Papers on influenza-associated aspergillosis (Cabug et al.) and severe ICU presentations (multiple case reports) reflect continuing evidence that viral infections—especially influenza—significantly increase risk for IA hospitalization and mortality.

6. Uncommon Presentations & Rare Pathogens

Reports of hydropneumothorax, prosthetic joint infection (A. penicillioides), endophthalmitis, and DiGeorge-associated aspergillosis show the wide clinical spectrum and the need for clinical suspicion—especially in immunocompromised hosts.

📚 Detailed Summaries of This Week’s Publications

1. Clinical Case Reports & Presentations

Tolosa-Hunt Syndrome Lookalikes Including Orbital Aspergillosis

Bommala S et al. | Cureus | 1 Dec 2025
DOI: https://doi.org/10.7759/cureus.74532
This case of painful ophthalmoplegia outlines key mimics of Tolosa-Hunt syndrome, including orbital aspergillosis, carotid–cavernous fistula, Burkitt lymphoma metastasis, and Miller-Fisher syndrome.
Key takeaway: Orbital aspergillosis remains an important differential in patients with severe unilateral headache and ocular motor palsies.

**Survival from A. terreus IPA on Sequential VA–VV ECMO**

Ordaz EGM | Research Square (preprint) | 28 Nov 2025
DOI (preprint): https://doi.org/10.21203/rs.3.rs-1127632/v1
Describes a critically ill patient requiring sequential extracorporeal support who survived proven invasive pulmonary aspergillosis (A. terreus).
Key takeaway: ECMO does not eliminate diagnostic challenges; persistent bronchoscopy and culture remain essential.

Recurrent Hydropneumothorax in CPA

Tang C et al. | BMJ Case Reports | 26 Nov 2025
DOI: https://doi.org/10.1136/bcr-2024-268568
An immunocompetent patient developed recurrent hydropneumothorax ultimately linked to chronic cavitary pulmonary aspergillosis.
Key takeaway: CPA may present with pleural complications such as hydropneumothorax, not only cavities or haemoptysis.

Bronchoscopic Appearance of Tracheobronchial Aspergillosis

Tapia Barredo L et al. | Med Intensiva | 27 Nov 2025
DOI: https://doi.org/10.1016/j.medin.2025.10.001
Provides macroscopic descriptions of TBA during bronchoscopy.
Key takeaway: Helps clinicians recognise TBA early, especially in ventilated or immunosuppressed patients.

Prosthetic Knee Joint Infection by Aspergillus penicillioides

Nakano H et al. | BMC Infect Dis | 24 Nov 2025
DOI: https://doi.org/10.1186/s12879-025-1645-8
A very rare cause of prosthetic joint infection, requiring prolonged antifungal therapy.
Key takeaway: Rare species can cause deep tissue infections; species identification and susceptibility testing essential.

2. Epidemiology & Burden

ABPA in Asthma–COPD Overlap (China)

Wang W et al. | Respiratory Medicine | 27 Nov 2025
DOI: https://doi.org/10.1016/j.rmed.2025.108547
Reports rates of ABPA in adults with both asthma and COPD.
Key takeaway: ACO populations may have significantly higher ABPA prevalence than asthma alone, suggesting under-recognition.

Aspergillosis-Related Mortality in the United States

Walsh TJ et al. | Clinical Infectious Diseases | 24 Nov 2025
DOI: https://doi.org/10.1093/cid/ciaf653
Analysis of national death certificates shows invasive aspergillosis frequently listed as a primary cause of death.
Key takeaway: High mortality persists, reinforcing the importance of early detection and aggressive management.

3. Diagnostics & Imaging

Molecular Diagnostics in Cancer Patients with Suspected IA

Rickerts V et al. | J Clin Microbiol | 26 Nov 2025
DOI: https://doi.org/10.1128/jcm.01201-25
Evaluates multi-target PCR and antigen testing in BAL and serum.
Key takeaway: Supports wider adoption of rapid molecular diagnostics in high-risk oncology settings.

Radiolabelled Siderophores for Aspergillosis Imaging

Dvorakova Bendova K et al. | npj Imaging | 26 Nov 2025
DOI: https://doi.org/10.1038/s44304-025-00163-y
Rat studies show radiolabelled siderophores accumulate specifically in infected lung tissue.
Key takeaway: Potential groundbreaking tool for early non-invasive localisation of IA lesions.

4. Immunology & Pathogenesis

Defective IFN-γ Responses in CPA

Janssen NAF et al. | J Infect Dis | 29 Nov 2025
DOI: https://doi.org/10.1093/infdis/jiaf596
CPA patients demonstrate impaired interferon-gamma production.
Key takeaway: Suggests a consistent, measurable immune defect—opening doors for immunomodulatory therapies.

Charcot–Leyden Crystals in ABPA (Preprint)

Aegerter H et al. | medRxiv | 27 Nov 2025
DOI: https://doi.org/10.1101/2025.11.27.1126628
Shows that CLCs are present in ABPA sputum and directly promote airway inflammation.
Key takeaway: CLCs are not passive by-products—they drive pathology, especially in mucus-plugging conditions.

IL-18Rα Expression and Viral–Fungal Interactions

Cabug AF et al. | Nat Commun | 24 Nov 2025
DOI: https://doi.org/10.1038/s41467-025-50342-1
Demonstrates how IL-18Rα high-expressing T cells influence severe viral disease and contribute to influenza-associated pulmonary aspergillosis.
Key takeaway: Connects viral immunopathology with susceptibility to IAPA.

5. Treatment & Resistance

Antifungal Susceptibility in Eastern India

Nikhil A et al. | MicrobiologyOpen | 1 Dec 2025
DOI: https://doi.org/10.1002/mbo3.70136
Includes 431 CPA isolates, plus ABPA and other pulmonary forms.
Key takeaway: Confirms significant regional variation in azole susceptibility—important for stewardship.

Off-label Use of Novel Antimicrobials

Retamar-Gentil P et al. | JAC-AMR | 24 Nov 2025
DOI: https://doi.org/10.1093/jacamr/dlaf184
Provides expert consensus on off-label antifungal use, including isavuconazole in refractory cases.
Key takeaway: Practical guidance for difficult-to-treat IA and mucormycosis.

IMI in Children – Progress & Barriers

Yeoh DK et al. | Clin Microbiol Infect | 27 Nov 2025
DOI: https://doi.org/10.1016/j.cmi.2025.11.015
Comprehensive review of invasive mould infections in paediatrics.
Key takeaway: Diagnostics remain limited; clinical suspicion remains essential.

6. Other Notable Reports

HES Mimicking ABPA/EGPA

Chakravarty K et al. | Oxf Med Case Rep | 26 Nov 2025
DOI: https://doi.org/10.1093/omcr/omaf238
Key takeaway: Eosinophilic disorders can closely mimic ABPA, requiring careful differential diagnosis.

Traumatic Fungal Endophthalmitis

Farnan R et al. | BMC Ophthalmol | 25 Nov 2025
DOI: https://doi.org/10.1186/s12886-025-0661-5
Key takeaway: Aspergillus and Fusarium remain major causes of post-traumatic fungal endophthalmitis.

22q11.2 Deletion Syndrome & Disseminated Aspergillosis

Liebling E et al. | Orphanet J Rare Dis | 24 Nov 2025
DOI: https://doi.org/10.1186/s13023-025-04041-x
Key takeaway: Severe immunodeficiency predisposes to disseminated fungal infection; vigilance required.

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

COVID Vaccines: Yes, There Is Some Risk — But COVID Infection Causes Far More Harm

People living with aspergillosis, CPA, ABPA, bronchiectasis, asthma or sarcoidosis often feel understandably anxious about vaccination.
Concerns about myocarditis, side effects, and frightening stories online are completely normal.

But when you compare the risks of the vaccine with the risks of COVID infection, a clear picture emerges:

⚠️ The vaccine carries some risk

🚨 COVID infection carries far, far more risk — and affects almost everyone

This article explains that difference clearly and honestly.

**1. COVID vaccines can cause harm — but this is rare**

No medical treatment is risk-free.
A very small number of people experience:

Fever
Fatigue
Headache
Swollen glands
Sore arm
Mild myocarditis (usually short-lived, rare, and mostly in young men)

Serious reactions such as hospitalisation or anaphylaxis are extremely rare — roughly 1–2 cases per million doses.

We should acknowledge this openly.

2. Almost everyone has had COVID in the last five years

Across the UK and most of the world, over 90% of adults now show antibodies from a past COVID infection, even if they didn’t realise they had it.

Many infections felt like a cold or passed unnoticed, but the body still experienced real risks:

heart inflammation
blood clots
lung inflammation
long-term fatigue
worsening of existing lung disease

Many people have had COVID more than once, and the risks increase with repeated infections.

So when we compare vaccine risk with infection risk, we’re not discussing a rare scenario — we are talking about something nearly everyone has already experienced, often multiple times.

3. COVID vaccines have prevented millions of hospitalisations and deaths

Global studies estimate that:

In the first year alone, COVID vaccines prevented around 19 million deaths worldwide.
WHO Europe reports more than 1.4 million lives saved in Europe alone.
A wider analysis suggests vaccines prevented over half of all potential hospitalisations and severe outcomes across many countries.

A simple way to think about it:

For every serious vaccine reaction, the vaccine prevents tens of thousands of hospitalisations and deaths.

This benefit is especially important for people with:

chronic lung disease
aspergillosis
bronchiectasis
asthma
immune suppression
long-term steroid use

For these groups, the protective effect of vaccination is greater than average, because COVID complications are more dangerous.

4. COVID infection causes far more harm than the vaccine

This is the crucial point.

COVID infection is 30–100 times more likely to cause myocarditis than the vaccine.

And infection-related myocarditis is:

more severe
more likely to require hospital care
more likely to leave long-term effects

COVID infection also increases the risk of:

blood clots
heart attacks
strokes
lung scarring
long COVID
ICU admission
worsening of asthma, ABPA, CPA and bronchiectasis

And the risk of death from infection is hundreds of times higher than the risk from vaccination.

5. Why scare stories feel louder than scientific facts

Scary individual stories spread quickly online.
But they are rare.

What we don’t see in the same dramatic way:

“Thousands of vulnerable patients avoided severe illness because they were vaccinated.”
“Vaccination prevented hospital admissions this week.”
“Most myocarditis cases after vaccination recover fully within days.”

Positive outcomes never go viral — but they happen constantly.

6. What this means for people with aspergillosis

COVID infection can:

trigger ABPA flares
worsen CPA cavities
increase mucus blockage
increase breathlessness
raise the risk of secondary fungal infections
accelerate lung damage
lead to hospitalisation

Vaccination significantly reduces all of these risks.

For most people with aspergillosis, vaccination is far safer than repeated COVID infections.

7. A supportive message for anyone still unsure

“It's true the vaccine carries some risk — all medicines do.
But COVID infection carries far, far more risk, and nearly everyone has had it at least once already.
Vaccination is the option that best protects your heart, your lungs, and your long-term health.”

by GAtherton

Fungal Vaccines: What New Research Could Mean for Aspergillosis Patients

Based on the 2025 Journal of Clinical Investigation commentary on emerging fungal vaccine science

jci-135-199451

Why fungal vaccines matter

Fungal infections remain a major global health problem, causing an estimated 3.8 million deaths per year. Yet despite this huge burden, there are currently no licensed vaccines to prevent or treat fungal disease.

For people living with aspergillosis—including chronic pulmonary aspergillosis (CPA), allergic bronchopulmonary aspergillosis (ABPA), severe asthma with fungal sensitisation (SAFS), and Aspergillus bronchitis—this gap is very real.
Treatments often involve long-term antifungal medications, steroids, or biologics, and symptoms may recur despite therapy.

A new scientific commentary in the Journal of Clinical Investigation highlights major progress in fungal vaccine research and suggests that vaccines may become important tools for both prevention and treatment in the future.

A new breakthrough: the Eng2 fungal antigen

Researchers studying serious fungal infections in North and South America have identified an enzyme called endoglucanase-2 (Eng2) that triggers a strong immune response:

It protected mice from Blastomyces, Histoplasma, and Coccidioides infections.
People recovering from these infections show memory CD4 T-cell responses to Eng2.

This suggests two important possibilities:

**1. A preventive vaccine**

A future vaccine could reduce the risk of developing serious fungal infections—especially in people with weakened immune systems or chronic lung disease.

**2. A therapeutic vaccine**

Unlike most vaccines, a therapeutic vaccine would be given after infection to support the immune system and help clearance—similar to how post-exposure rabies or hepatitis A vaccines work.

This second application is particularly relevant to aspergillosis.

Why fungal vaccines may be especially useful in Aspergillus disease

Although the study did not focus on Aspergillus specifically, the commentary highlights several reasons why Aspergillus vaccines are scientifically realistic.

1. Fungi are surprisingly easy to vaccinate against in animal studies

Many fungal antigens have already shown strong protective effects in experimental models.

Unlike viruses such as HIV or tuberculosis—where vaccines are extremely difficult—fungal pathogens often respond well to:

Antibody-based immunity
T-cell immunity

Both would be valuable in Aspergillus-related disease.

2. Aspergillosis mainly affects people with weakened or inflamed lungs

This makes it exactly the kind of disease where a vaccine could:

Reduce fungal burden in the airways
Decrease inflammation
Support existing treatments
Reduce flare-ups and symptoms

3. A therapeutic vaccine may arrive before a preventive vaccine

Chronic fungal diseases (especially CPA and Aspergillus bronchitis) develop slowly and persist for months or years.
This gives time for a vaccine to stimulate the immune system during ongoing treatment.

A therapeutic vaccine could:

Enhance the effect of antifungal drugs
Reduce the amount of fungus growing in cavities or bronchiectatic airways
Lower inflammation and antibody levels
Potentially reduce the need for long-term steroids or biologics in ABPA

4. A combination (“multivalent”) vaccine is possible

The Eng2 research shows that one antigen may not protect against all fungal species.
However, a “cocktail” vaccine—using several fungal proteins—could cover multiple fungi, including Aspergillus.

What this could mean for different aspergillosis conditions

For CPA (Chronic Pulmonary Aspergillosis)

A therapeutic vaccine might help:

Reduce fungal load in cavities
Improve long-term control
Support patients who can’t tolerate antifungals
Reduce reliance on prolonged azole therapy

For ABPA (Allergic Bronchopulmonary Aspergillosis)

ABPA is an allergic reaction rather than a true infection.
But reducing the amount of Aspergillus in the airways could:

Decrease IgE levels
Reduce flare frequency
Lower the need for steroids
Improve asthma control

For SAFS and Aspergillus bronchitis

A vaccine could potentially:

Reduce airway colonisation
Improve symptom control
Reduce the cycle of infection → inflammation → airway damage

What this means for patients today

It is important to be clear:

There is no Aspergillus vaccine available yet.

However, the science is moving faster than ever.
The commentary highlights:

Multiple experimental vaccines have already worked in animals
Some fungal vaccines have reached early human trials
mRNA technology (used for COVID vaccines) could accelerate development
High-risk groups—including people with chronic lung disease—would be early candidates

For the aspergillosis community, this research is a major step forward, offering hope for safer and more effective long-term management.

For clinicians: why this matters now

Non-specialist clinicians may want to be aware that:

Vaccine-based immunotherapy may become part of fungal disease management
Therapeutic vaccines could work alongside antifungals, rather than replacing them
Advances in antigen identification (e.g., Eng2) create realistic pathways for Aspergillus-specific research
Patient groups with chronic fungal or allergic disease may benefit significantly from immunological boosting

As fungal disease continues to rise worldwide, vaccination represents a promising future tool in managing both invasive and chronic fungal illnesses.

Looking ahead

While fungal vaccines are “so needed, so feasible, and yet still far off,” the momentum is building.
For people living with aspergillosis—often for many years—the possibility of vaccines offers genuine hope for:

Better control
Improved quality of life
Reduced treatment burden
Less risk of long-term complications

This new research marks an important step on that journey.

by GAtherton

🌐 Promoting the NHS National Aspergillosis Centre (NAC)

Nationally Commissioned Service • Specialist Advice • Remote MDT • Patient Support

Chronic and allergic aspergillosis remain significantly under-recognised across the UK — despite their substantial burden on respiratory, infectious disease, and immunology services.

As the NHS England–commissioned National Aspergillosis Centre (NAC), based at Wythenshawe Hospital (Manchester University NHS Foundation Trust), we provide national expertise, remote support, and shared-care pathways for clinicians managing these complex conditions.

📊 Why This Matters

Chronic pulmonary aspergillosis (CPA) affects an estimated 3–4 per 100,000 people in the UK, with far higher rates in those with:

Previous tuberculosis
COPD
Non-tuberculous mycobacterial (NTM) lung disease
Sarcoidosis
Bronchiectasis

Allergic bronchopulmonary aspergillosis (ABPA) may affect:

2.5% of adult asthmatics
Up to 15% of people with cystic fibrosis

Yet both conditions are frequently undiagnosed or misdiagnosed, leading to delayed treatment and avoidable morbidity.

🏥 How NAC Supports Clinicians Across the UK

As the nationally commissioned centre for chronic aspergillosis, we offer:

🩺 Specialist clinical care

Face-to-face and remote clinics with structured long-term follow-up in partnership with local teams.

👥 National Aspergillosis MDT via Teams Remote Communication

A dedicated MDT where clinicians can refer and discuss complex diagnostic or therapeutic cases.

📧 Consultant-led advice & guidance

Available via phone & email, including:

Diagnostic support
Interpretation of IgE/IgG and fungal microbiology
Antifungal prescribing advice
Case planning for ABPA, CPA, SAFS and Aspergillus bronchitis

🔬 Access to advanced diagnostics

Including Aspergillus-specific IgE/IgG, culture, imaging, and molecular testing (e.g. antifungal resistance).

💬 Patient support & education (NAC CARES)

Moderated online groups, weekly patient meetings, webinars, and comprehensive educational resources — helping patients understand their condition and remain safely supported close to home.

🤝 We Welcome Collaboration

We’d be pleased to connect with respiratory, ID, immunology, and internal medicine teams to discuss:

Shared-care pathways
Diagnostic support
Service guidance
Virtual or in-person educational sessions
Case-specific MDT referrals

📄 Further information

Referral pathways, service scope and patient resources:
👉 https://mft.nhs.uk/wythenshawe/services/infectious-diseases/national-aspergillosis-centre/

Dr Chris Kosmidis
Clinical Lead, NHS National Aspergillosis Centre
Manchester University NHS Foundation Trust

by GAtherton

🌡️ 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.

by GAtherton

⭐ 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)

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/
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)
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/
Voriconazole N‑oxide metabolite in TDM (case)
Farm Hosp (2025) — Orozco Cifuentes I et al.
PMID: 41274859
https://pubmed.ncbi.nlm.nih.gov/41274859/
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
IL‑37 in respiratory disease (incl. aspergillosis models) — review
Front Immunol (2025)
PMCID: PMC12640846
https://europepmc.org/article/PMC/12640846
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
Expert consensus: off‑label/novel antimicrobials (aspergillosis contexts cited)
JAC Antimicrob Resist (2025)
PMCID: PMC12641089
https://europepmc.org/article/PMC/12641089
ABPA with pleuro‑parenchymal aspergillus infection — case
J Postgrad Med (2025) — Spalgais S et al.
PMID: 41277380
https://pubmed.ncbi.nlm.nih.gov/41277380/
Aspergillus endophthalmitis post‑phaco — failed salvage — case
Int Ophthalmol (2025) — Huang Z
PMID: 41247646
https://pubmed.ncbi.nlm.nih.gov/41247646/
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
Mold pneumonia in resource‑limited Asia — Delphi consensus
Med Mycol (2025) — Asia Fungal Working Group
PMID: 41251327
https://pubmed.ncbi.nlm.nih.gov/41251327/
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/
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/
Destroyed lung pneumonectomy — complications; CPA/haemoptysis associations
J Surg Res (2025) — Yu L et al.
PMID: 41270587
https://pubmed.ncbi.nlm.nih.gov/41270587/
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/
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
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
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
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
SFTS complicated by IPA — prediction nomogram
BMC Infect Dis (2025) — Yan R et al.
PMID: 41275152
https://pubmed.ncbi.nlm.nih.gov/41275152/
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
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
Preprint: antibiotics → impaired neutrophil anti‑Aspergillus immunity (mouse)
BioRxiv (2025) — Aufiero MA & Hohl TM
PPR: PPR1122060
https://www.biorxiv.org/ (search PPR1122060)
Preprint: HosA HDAC in A. fumigatus virulence
BioRxiv (2025) — Liu H et al.
PPR: PPR1121973
https://www.biorxiv.org/ (search PPR1121973)
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
Clove (S. aromaticum) essential oil in rabbit aspergillosis — preclinical
Research Square (2025) — Shokrpoor S et al.
PPR: PPR1121622
https://www.researchsquare.com/ (search PPR1121622)
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

by GAtherton

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

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

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

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

This article explains what we know so far.

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

ABPA is mainly an allergic reaction to Aspergillus in the airways.
CPA is a chronic fungal infection that causes cavities, scarring, and long-term lung damage.
Some people start with ABPA and later develop CPA, or the two conditions overlap.
The 2024 international ABPA guidelines now recognise this overlap as real and important.

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

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

Biologics can help patients with ABPA or severe asthma by:

reducing steroid use
improving breathing
decreasing mucus plugging
lowering flare-ups
improving quality of life

Biologics most commonly used in ABPA include:

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

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

⚠️ 3. Biologics and CPA: much less evidence

CPA is caused by persistent fungal infection and structural lung damage.
Biologics do not treat fungal infection, and they do not prevent cavities.
In CPA, the mainstay of treatment is still:
- antifungal medication (usually itraconazole, voriconazole or posaconazole)
- careful imaging (CT scans)
- airway clearance
- sometimes surgery or bronchoscopy

There is no strong evidence that biologics help CPA itself.

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

This is where things become more complex.

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

they do not treat fungal infection
they do not stop fungal cavities from progressing
they may reduce inflammation that normally helps the body contain infection

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

Specialist centres (like the NAC) now emphasise:

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

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

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

⭐ Most promising for ABPA:

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

⭐ Increasing interest:

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

⭐ Useful in selected cases:

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

⚠️ Uncertain in CPA:

None of the biologics treat fungal infection or cavities directly.
Their role in active CPA remains unclear and requires careful oversight.

🧭 6. What this means for patients

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

steroids cause side-effects
your asthma is uncontrolled
you have frequent flare-ups
your IgE levels are very high
mucus plugging or wheezing continues despite treatment

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

antifungal medication usually needs to continue
biologics may still help if the allergic component is significant
CT scans must be repeated to make sure cavities are not progressing
specialists must weigh benefits vs. risk for each patient individually

💬 7. Summary

Biologics can be extremely helpful for ABPA.
They do not treat CPA, and cannot replace antifungal medicines.
In patients with both ABPA and CPA, the approach must be personalised.
Dupilumab and (possibly) tezepelumab are emerging biologics with promise, but evidence is still developing.
Decisions should always be made with a specialist centre such as the National Aspergillosis Centre (NAC).

by GAtherton