⭐ Aspergillus Bronchitis: The Overlooked Condition Hiding in Plain Sight
Estimated prevalence 1–2% in bronchiectasis and chronic airway disease clinics.
Aspergillus Bronchitis (AB) is a chronic, symptomatic infection of the airways caused by Aspergillus species in people with underlying lung disease. It sits between simple colonisation and chronic pulmonary aspergillosis (CPA), and is frequently overlooked or mislabelled as “recurrent infection,” “post-viral symptoms,” or uncontrolled bronchiectasis.
Unlike CPA, Aspergillus Bronchitis does not require cavities or major structural destruction — which makes it both easier to miss and surprisingly common among people with chronic airway disease.
When recognised and treated (usually with antifungal therapy for several months), symptoms often improve significantly. But because awareness remains low, most patients cycle through unnecessary antibiotics, repeated exacerbations, and worsening airway disease before the real cause is identified.
⭐ What Exactly Is Aspergillus Bronchitis?
Aspergillus Bronchitis is defined by:
-
chronic productive cough
-
sputum growing Aspergillus species repeatedly
-
airway inflammation
-
symptoms lasting over 3 months
-
underlying airway disease (bronchiectasis, CF, COPD, prior TB, ABPA)
-
response to antifungal therapy
Unlike ABPA:
-
there is no allergic response,
-
IgE is usually normal,
-
eosinophils are normal or mildly elevated.
Unlike CPA:
-
there are no cavities on imaging,
-
IgG may be normal or only slightly elevated,
-
disease is confined to the airways, not lung tissue.
This places AB in a “grey zone” — often invisible unless specifically looked for.
⭐ Why Aspergillus Bronchitis Is Missed
1. Symptoms mimic common chronic airway disease
Typical AB symptoms include:
-
daily productive cough
-
worsening sputum thickness
-
breathlessness
-
fatigue
-
repeated “chest infections”
-
slow-to-clear mucus
-
crackles or wheeze
These resemble:
-
bronchiectasis exacerbations
-
COPD flare-ups
-
chronic infection with Pseudomonas or NTM
-
post-viral cough
-
uncontrolled asthma
Without fungal awareness, clinicians default to bacterial explanations.
2. Sputum grows multiple organisms — Aspergillus is dismissed
In bronchiectasis, sputum frequently grows:
-
Haemophilus
-
Pseudomonas
-
Staphylococcus
-
Streptococcus
-
NTM
When Aspergillus appears, it’s often labelled:
-
“colonisation”
-
“contaminant”
-
“not clinically relevant”
But repeated isolation with persistent symptoms is highly suggestive of AB.
3. IgE/IgG results may be normal
Many clinicians expect high IgE or IgG to “confirm Aspergillus disease.”
But in Aspergillus Bronchitis:
-
IgE is usually normal
-
IgG can be normal or borderline
This leads to false reassurance.
4. Radiology rarely shows overt features
CT scans in AB may show:
-
mucus plugging
-
mild bronchial wall thickening
-
small nodules
-
progression of bronchiectasis
But they do not show the cavities of CPA or classic features of ABPA.
Therefore radiologists often report scans as “no significant change” or “stable bronchiectasis.”
5. Antibiotics appear to help — temporarily
Patients often improve slightly with:
-
amoxicillin
-
doxycycline
-
macrolides
-
ciprofloxacin
This gives clinicians the impression of bacterial disease, but symptoms soon return.
6. Lack of awareness
Many specialists (even in respiratory clinics) are unaware that Aspergillus Bronchitis:
-
exists as a distinct clinical entity
-
can be disabling
-
responds to antifungals
-
predicts progression to CPA if untreated
This leads to significant diagnostic delay.
⭐ Who Is at Highest Risk?
1. Bronchiectasis
The largest risk group.
Aspergillus Bronchitis may account for 1–2% of all bronchiectasis patients, and up to 5–10% in severe or frequent exacerbator groups.
2. Cystic Fibrosis (CF)
These patients frequently grow Aspergillus but not all have ABPA — some have Aspergillus Bronchitis.
3. COPD and chronic productive cough
Especially those with:
-
frequent mucus plugging
-
repeated “infective exacerbations”
-
progressive sputum production
4. Post-TB airway damage
Chronic airway deformity, scarring, and bronchiectasis from old TB predispose to fungal infection.
5. Post-COVID structural disease
A new and growing risk group, especially after prolonged ICU ventilation.
6. ABPA patients
Some patients develop Aspergillus Bronchitis during steroid-dominated treatment or after stopping antifungals.
⭐ Which Specialities Need Greater Awareness?
-
Respiratory medicine
(especially bronchiectasis clinicians and severe asthma teams) -
Infectious Diseases
(frequent respiratory presentations with chronic airway infection) -
Radiology
(to recognise subtle but progressive airway changes) -
Primary care
(“recurrent chest infection” or “persistent cough” patients) -
Physiotherapy & airway clearance teams
(excessive sputum with fungal elements) -
Cystic Fibrosis services
The National Aspergillosis Centre is the ideal referral destination when diagnosis is uncertain or symptoms persist despite typical management.
⭐ Red Flags Suggesting Aspergillus Bronchitis
1. Chronic (>3 months) productive cough + repeated Aspergillus in sputum
Even 2 positive sputums in the right clinical context should raise suspicion.
2. Bronchiectasis patient not improving on repeated antibiotics
3. Thick, tenacious mucus with black, grey, or brown plugs
4. Worsening CT bronchiectasis or mucus plugging
5. Absence of features typical for ABPA (normal IgE, no fleeting infiltrates)
6. Asthma or COPD patient with new persistent sputum
7. Partial response to antibiotics but rapid relapse
8. Unexplained fatigue and breathlessness in someone with airway disease
⭐ The Cost of Missed Aspergillus Bronchitis
If AB is not recognised early, consequences include:
-
repeated exacerbations
-
accelerating bronchiectasis
-
long-term airway damage
-
chronic inflammation
-
steroid overuse
-
unnecessary antibiotics
-
repeated hospitalisations
-
progression to CPA in some patients
For health systems, missed diagnosis leads to:
-
higher admission rates
-
inappropriate long-term antibiotic use
-
avoidable CT scans and investigations
-
greater long-term burden of CPA
But antifungal therapy — when appropriately used — can offer marked symptom improvement and reduce exacerbation frequency.
⭐ Conclusion
Aspergillus Bronchitis is a distinct, treatable form of chronic airway disease seen in people with bronchiectasis, asthma, COPD, CF, and post-TB lung damage. Yet lack of awareness means many patients are repeatedly misdiagnosed with bacterial infections or unexplained chronic cough.
Recognising red flags, reviewing sputum results carefully, and considering antifungal therapy can dramatically improve outcomes. Early referral to specialist centres such as the National Aspergillosis Centre is recommended for complex cases or uncertain diagnosis.
Early identification prevents airway deterioration — and reduces the likelihood of progression to CPA.
⭐ Allergic Bronchopulmonary Aspergillosis (ABPA): Why Diagnosis Is Missed and Who Needs to Be More Aware
With estimated prevalence of 1–2% in asthma clinics and up to 10% in severe asthma services.
Allergic Bronchopulmonary Aspergillosis (ABPA) is a chronic immune reaction to Aspergillus that affects people with asthma or cystic fibrosis. It causes airway inflammation, mucus plugging, recurrent exacerbations, and bronchiectasis if untreated.
Despite being treatable, ABPA remains heavily underdiagnosed, even in countries with advanced respiratory services. Many people are told for years that they have “difficult asthma” or “recurrent chest infections,” only for ABPA to be diagnosed much later, often with significant lung damage already present.
The UK National Aspergillosis Centre (NAC) provides specialist expertise, yet only a small proportion of expected ABPA cases reach specialist review.
This article explains why ABPA is missed, which patients are at risk, which specialities need to be more alert, and the red flags that should prompt testing or referral.
⭐ How Common Is ABPA?
ABPA is more common than most clinicians realise:
| Population | Estimated prevalence |
|---|---|
| General asthma | 1–2% |
| Severe asthma clinics | 3–10% |
| Cystic fibrosis | 5–15% |
| Bronchiectasis (non-CF) | 1–4% |
Across the UK, this equates to an estimated 15,000–25,000 people living with ABPA — but only a small minority ever receive the correct diagnosis.
⭐ Why ABPA Is Often Missed
1. ABPA looks like “difficult asthma”
Typical symptoms — wheeze, cough, mucus, breathlessness — mimic:
-
severe asthma
-
eosinophilic asthma
-
uncontrolled asthma despite treatment
Patients may be repeatedly stepped up through inhalers, oral steroids, and biologics before ABPA is even considered.
2. Exacerbations are mistaken for infections
Many ABPA flare-ups are treated as:
-
pneumonia
-
viral infection
-
“chest infection”
-
post-viral asthma worsening
Without fungal-specific thinking, the diagnosis is rarely made.
3. IgE and eosinophils fluctuate
IgE is a cornerstone of ABPA diagnosis, but:
-
systemic steroids suppress IgE
-
biologics (benralizumab, mepolizumab, dupilumab) reduce eosinophils
-
flare-ups produce temporary spikes
-
baseline ranges vary between labs
Clinicians often overlook ABPA in patients on biologics because eosinophils are normal — despite the underlying fungal allergy still being active.
4. Radiology findings get mislabelled
ABPA causes:
-
mucus plugging
-
“tram lines” and bronchial thickening
-
fleeting infiltrates
-
upper lobe bronchiectasis
These are often:
-
labelled “infection”
-
attributed to asthma airway remodelling
-
not compared across time
-
missed on CT unless specifically looked for
5. Inconsistent awareness across specialities
Some clinicians are unfamiliar with:
-
ISHAM diagnostic criteria
-
interpreting IgE/IgG results
-
the relationship between asthma and fungal allergy
-
the overlap between ABPA and bronchiectasis
This leads to diagnostic delay or misdiagnosis.
6. ABPA evolves into chronic disease if untreated
Repeated inflammation → mucus plugging → bronchiectasis → fibrosis.
By the time a diagnosis is made, airway damage can be permanent.
⭐ Who Is at Highest Risk?
1. Asthma patients with repeated exacerbations
Especially those who:
-
fail maximal inhaler therapy
-
require multiple steroid courses
-
have sudden, dramatic mucus plugging events
-
experience episodic “flares” with no clear cause
2. Severe asthma clinic patients
Prevalence is up to 10%, especially those with:
-
high IgE
-
eosinophilia
-
sensitisation to multiple allergens
-
steroid dependence
3. Bronchiectasis patients
Bronchiectasis often coexists with ABPA and can worsen flares.
4. Patients with mucus plugging (“finger-in-glove” signs)
These striking CT appearances strongly suggest ABPA but are often misattributed to infection.
5. People with CF (Cystic Fibrosis)
5–15% develop ABPA at some stage.
⭐ Which Specialities Need Greater Awareness?
-
Severe asthma services & biologics clinics
(highest yield group for ABPA detection) -
Respiratory medicine
(diagnosis often falls here but is highly variable) -
General practice
(sees frequent “exacerbations”) -
Emergency departments & acute medical units
(manage acute mucus plugging, chest tightness) -
Paediatric respiratory medicine
(early recognition prevents chronic damage) -
Cystic Fibrosis services
-
Radiology
(fleeting infiltrates and mucus plugging often give the earliest clues)
The National Aspergillosis Centre should be the referral point for complex or uncertain cases.
⭐ Red Flags Suggesting ABPA
1. Asthma with repeated, unexplained exacerbations
Especially if poorly responsive to normal treatment.
2. High total IgE (>500–1000 IU/mL)
Or rising IgE over time.
3. Eosinophilia (unless suppressed by treatment)
4. Positive Aspergillus sensitisation
(Skin prick test or specific IgE)
5. Bronchiectasis, particularly central or upper lobe
6. Fleeting pulmonary infiltrates
7. Mucus plugging on CT (“finger-in-glove” appearance)
8. ABPA flare triggered by stopping antifungals
9. Asthma + Aspergillus in sputum
⭐ The Cost of Missed ABPA Diagnosis
Failure to diagnose ABPA leads to:
-
progressive airway damage
-
permanent bronchiectasis
-
steroid dependence
-
hospital admissions
-
repeated infections
-
respiratory failure in advanced stages
-
reduced quality of life
-
avoidable healthcare expenditure
Delayed diagnosis increases the risk of progression to CPA, a far more serious chronic fungal infection requiring long-term antifungal therapy.
Early recognition, correct treatment, and referral to specialist centres like the National Aspergillosis Centre dramatically improve long-term outcomes.
⭐ Conclusion
ABPA is not rare — especially within severe asthma clinics, bronchiectasis services, and CF units. Yet it remains significantly underdiagnosed because its symptoms mirror those of common respiratory conditions, and because key investigations like IgE, IgG, and CT interpretation are inconsistently used.
A structured approach — recognising red flags, performing appropriate testing, and referring complex cases to the National Aspergillosis Centre — can reduce the burden of avoidable airway damage and improve the lives of thousands of patients.
⭐ Chronic Pulmonary Aspergillosis: Why Diagnosis Is Missed and Who Needs to Be More Aware
With estimated prevalence of 3–4 cases per 100,000 population, and far higher rates in high-risk groups.
Chronic Pulmonary Aspergillosis (CPA) is a slowly progressive fungal lung disease affecting an estimated 3–4 per 100,000 people in the UK, with higher estimates in global settings with greater TB prevalence. Despite this, many clinicians will go through entire careers without confidently recognising it — not because it is extremely rare, but because it almost always hides inside other long-term lung diseases.
The UK is unusual in having a nationally commissioned specialist service — the National Aspergillosis Centre (NAC), based at Wythenshawe Hospital, Manchester — offering funded diagnostics, multidisciplinary review, and long-term antifungal management. But only a fraction of expected CPA cases are ever referred. Most are simply never diagnosed.
This article explains why diagnoses are missed, who is at highest risk, which specialities need to be more alert, and the red flags that should trigger testing or referral.
⭐ How Common Is CPA? The Numbers Behind the Problem
The UK prevalence is estimated at 3–4 per 100,000 people — approximately 2,000–2,500 people with CPA at any given time.
But the risk is far higher in specific groups:
| Risk Group | Estimated CPA prevalence |
|---|---|
| Post-TB lung disease | 6–10% in those with residual cavities |
| Severe COPD (GOLD III–IV) | 1–3% |
| Bronchiectasis | 1–3% |
| NTM disease | 3–10% |
| Sarcoidosis with fibrosis | 1–2% |
| Immunosuppression (steroids/biologics) | Unknown, but rising |
Using these figures, the true UK caseload could exceed 4,000–6,000 individuals, yet NAC receives ~500–1,000 referrals, highlighting a large diagnostic gap.
⭐ Why CPA Is So Often Missed
1. Symptoms mimic common chronic lung diseases
CPA presents with:
-
Persistent cough
-
Breathlessness
-
Fatigue
-
Weight loss
-
Recurrent “chest infections”
-
Haemoptysis
These overlap almost perfectly with:
-
COPD
-
bronchiectasis
-
post-TB changes
-
long COVID
-
NTM infection
-
repeatedly “slow to clear” pneumonia
Because symptoms are non-specific, clinicians rarely think fungal.
2. Interpretation of imaging is inconsistent
CPA shows:
-
one or more cavities
-
pleural thickening
-
nodules
-
progressive changes over months
-
fungal balls
Common reporting pitfalls:
-
labelled “post-infective scarring”
-
misinterpreted as malignancy
-
seen but not compared longitudinally
-
incidental CT findings not acted upon
Radiology is one of the biggest missed opportunities for early detection.
3. IgG testing is not routinely requested
Aspergillus IgG is the key diagnostic biomarker — but it is:
-
often confused with IgE
-
not available in some hospitals
-
omitted from workups for recurrent infection
-
unfamiliar to non-respiratory clinicians
Without IgG, CPA is rarely diagnosed.
4. Short-term improvement with antibiotics is misleading
Patients with CPA may temporarily feel better after:
-
broad-spectrum antibiotics
-
steroids
-
physiotherapy
This transient improvement creates false reassurance.
5. CPA spans multiple specialisms — and no one owns it
Diagnosis requires combined expertise across:
-
respiratory medicine
-
infectious diseases
-
radiology
-
microbiology
-
immunology
When no one speciality takes responsibility, patients get lost.
⭐ Which Patients Are at High Risk?
CPA almost always develops on a background of existing lung damage.
1. Post-TB lung disease (PTLD)
Globally the largest CPA population.
Residual cavities are the strongest predictor.
Specialities needing awareness:
-
TB teams
-
ID physicians
-
Radiologists
-
Community TB nurses
-
Public health TB programmes
2. COPD (especially severe / emphysema)
Millions of people are potentially at risk.
Recurrent infections + bullae/cavities = fertile ground for CPA.
Specialities:
-
COPD clinics
-
Pulmonary rehab
-
Acute medicine (frequent admissions)
3. Bronchiectasis
Damaged airways enable persistent Aspergillus colonisation and inflammation.
Specialities:
-
Bronchiectasis MDTs
-
Severe asthma & NTM clinics
-
Respiratory physiotherapy
4. Sarcoidosis and ILD
Fibrosis and traction bronchiectasis develop cavities over time.
5. Post-COVID or post-influenza structural disease
Emerging risk group, especially in patients with:
-
ventilatory lung injury
-
persistent CT abnormalities
-
chronic steroid exposure
6. Chronic steroid or immunomodulator use
While invasive aspergillosis is linked to profound immunosuppression, CPA often affects those with milder, chronic immune dysfunction:
-
systemic steroids
-
high-dose inhaled steroids
-
biologics affecting eosinophils
-
poorly controlled diabetes
-
chronic kidney disease
-
malnutrition
⭐ Which Specialities Need to Be More Alert?
-
Respiratory Medicine – primary detection, but awareness varies greatly
-
Infectious Diseases – especially post-TB and persistent infection clinics
-
Radiology – key to spotting early changes
-
Primary Care – sees patients repeatedly with “ongoing chest infections”
-
Emergency & acute medicine – haemoptysis presentations
-
Bronchiectasis and NTM services – strong overlap
-
Severe asthma and biologics teams – ABPA → CPA evolution
-
TB clinics – highest prevalence globally, often least recognised
The National Aspergillosis Centre should be the referral point for any complex or uncertain case.
⭐ Red Flags: When to Suspect CPA
1. Cavities on CT (thin-, thick-walled, evolving, or multiple)
Especially with pleural thickening.
2. Haemoptysis
CPA is one of the most common causes of haemoptysis in people with cavities.
3. Symptoms lasting >3 months
Chronic cough, fatigue, weight loss, breathlessness.
4. “Recurrent infections” that never fully resolve
5. Post-TB patient with any new or worsening symptoms
6. Bronchiectasis patient with new cavity or Aspergillus culture
7. High or rising Aspergillus IgG
8. ABPA patient who deteriorates off antifungals
⭐ The Cost of Missed Diagnoses
When CPA is not recognised early, the consequences are severe:
-
irreversible lung damage
-
repeated hospitalisations
-
emergency haemoptysis events
-
prolonged antifungal therapy with more toxicity
-
reduced quality of life
-
avoidable deaths
For systems like the NHS, late diagnosis increases costs:
-
unplanned admissions
-
repeated CT imaging
-
prolonged antibiotics
-
intensive care during haemoptysis
-
complex surgery (lobectomy/pneumonectomy)
Early referral to specialist centres like the National Aspergillosis Centre prevents many of these harms.
⭐ Conclusion
CPA is not rare within the populations most likely to develop it.
Missed diagnoses are common, predictable, and preventable.
By increasing awareness across Respiratory, Infectious Diseases, Radiology, Primary Care, TB services, and severe asthma pathways — and by using simple tools such as Aspergillus IgG and careful CT interpretation — clinicians can dramatically reduce the diagnostic delay that damages lungs, quality of life, and survival.
The UK is fortunate to have the National Aspergillosis Centre as a nationally commissioned referral service. Recognising CPA early and referring appropriately has the power to save lives, reduce system costs, and improve long-term outcomes.
🌐 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
🧩 NAC Aspergillosis Research Digest Aspergillosis (October 2025: week 43)
Highlights
- Post‑transplant GVHD & IFI risk: In paediatric liver transplant recipients with GVHD, invasive fungal infection (aspergillosis/candidiasis) was the dominant cause of death; paper advocates PK‑guided monitoring of JAK inhibitors and tacrolimus for safer immunosuppression. (Pediatr Transplant; free full text) PMID: 41039701 | PMCID: PMC12491760
- Inhaled opelconazole: In‑vitro + clinical data suggest negligible drug–drug interaction (DDI) risk for the investigational inhaled triazole opelconazole, supporting development for pulmonary aspergillosis. (JAC) PMID: 41105437
- Isavuconazole DDI mapping: PBPK modelling compares isavuconazole with other azoles and proposes model‑informed dosing for anticancer drugs—useful in haem‑onc co‑prescribing. (CPT:PSP) PMID: 41104611
- CAR‑T fungal infections: Registry analysis after CD19 CAR‑T for B‑cell lymphoma reports invasive aspergillosis as the commonest mould IFI (11/32). (CMI) PMID: 41109429
- Air pollution & IPA: Two multicentre cohorts link higher fine particulate (PM2.5) exposure before admission with invasive pulmonary aspergillosis in severe pneumonia. (EBioMedicine) PMID: 41106023
- Mechanisms of resistance/virulence: A bioRxiv preprint identifies a long non‑coding RNA (afu‑182) that modulates triazole susceptibility and virulence in A. fumigatus. (Preprint) PPR: PPR1101933
- Burden estimates (Poland): National modelling updates burden for IA, CPA, ABPA, SAFS—useful for service planning and advocacy. (Sci Rep; open) PMID: 41087447 | Full text
Diagnostics
- Dental/ENT interface: In a retrospective implant‑centred series, chronic sinusitis and aspergillosis were histopathologically confirmed in a subset of sinus augmentation candidates; authors discuss when 3D imaging is warranted pre‑procedure. (Int J Oral Maxillofac Implants) PMID: 41105467
- Environmental surveillance: Post‑hurricane housing study identified Aspergillus spp. in water‑impacted homes, contextualising environmental exposure risk for ABPA/CPA. (Sci Rep; open) PMID: 41087584
Therapeutics & stewardship
- Opelconazole (inhaled triazole) DDI profile appears favourable (see above). Consider future role for adjunct/targeted lung delivery once efficacy data mature. PMID: 41105437
- Isavuconazole PBPK‑based recommendations may aid co‑administration with anticancer agents; still requires centre‑specific DDI checks and, where available, TDM. PMID: 41104611
- Novel antifungal target: A selective acetyl‑CoA synthetase inhibitor shows antifungal activity in Nat Commun—early‑stage discovery but potentially relevant to future azole‑resistant IA/CPA. (Nat Commun; open) PMID: 41087359
Epidemiology & special populations
- CAR‑T recipients: IA predominance among mould IFIs underscores the need for surveillance, rapid diagnostics (GM/PCR), and early therapy in post‑CAR‑T care pathways. PMID: 41109429
- Air quality: Association between PM2.5 and IPA suggests including environmental history in risk assessments for severe pneumonia patients. PMID: 41106023
- Veterinary reservoir: Review from Turkey highlights aspergillosis as a major poultry disease—relevance for occupational exposures and broader One‑Health messaging. (Vet Med Sci; open) PMID: 40988581
Surgery & case‑based learning
- CPA with infected bulla: Case report supports surgical resection as an option in selected CPA phenotypes with localised disease. (Clin Case Rep; open) PMID: 41103592
Guidance / practice notes
- For post‑transplant GVHD, ensure PK monitoring (tacrolimus, JAK inhibitors) and early IFI screening (GM/LFA ± PCR) to balance GVHD control against infection risk. PMID: 41039701
- In CAR‑T and severe pneumonia pathways, include combined diagnostics (BAL GM, Aspergillus PCR ± culture) and rapid initiation of active triazoles where IA is probable.
- Consider air quality and environmental exposures (post‑disaster housing, poultry) in patient education and prevention.
References & links
- Sawada K et al. PK Monitoring of JAK Inhibitor and Tacrolimus in post‑LT GVHD. Pediatr Transplant. 2025. PMID: 41039701 | PMCID: PMC12491760
- Cass LMR et al. Opelconazole DDIs. J Antimicrob Chemother. 2025. PMID: 41105437
- Goosen TC et al. Isavuconazole DDI PBPK. CPT: Pharmacometrics Syst Pharmacol. 2025. PMID: 41104611
- Bouvier A et al. IFIs after CD19 CAR‑T. Clin Microbiol Infect. 2025. PMID: 41109429
- Zhou H et al. PM2.5 & IPA. EBioMedicine. 2025. PMID: 41106023
- Poudyal NR et al. lncRNA afu‑182 & azole susceptibility. bioRxiv. 2025. Preprint
- Tamagawa K et al. Lung resection in CPA with infected bulla. Clin Case Rep. 2025. PMID: 41103592
- Vélez‑Torres LN et al. Aspergillus in water‑impacted homes. Sci Rep. 2025. PMID: 41087584
- Krzyściak PM et al. Burden of serious mycoses in Poland. Sci Rep. 2025. PMID: 41087447
- Alhassani ANA et al. Aspergillosis in poultry (Turkey). Vet Med Sci. 2025. PMID: 40988581
Mannose-Binding Lectin (MBL) Deficiency and Aspergillosis
What is MBL?
Mannose-binding lectin (MBL) is a natural protein made by the immune system. Its job is to help the body recognise and fight off germs, including fungi like Aspergillus. It’s part of the “innate” immune system – the first line of defence you’re born with.
How common is MBL deficiency?
MBL deficiency is surprisingly common.
-
Around 5–10% of people have very low or absent levels.
-
If you include milder reductions, as many as 20–30% of people carry genetic changes that lower MBL activity.
For most, this causes no problems because the immune system has other pathways to fall back on. People often never know they have it.
Why do MBL levels vary?
-
Genetics: The MBL2 gene comes in different versions, some producing plenty of MBL and others producing little or none.
-
Inheritance: The combination of gene copies from each parent determines your level.
-
Normal diversity: Low levels are common and often harmless, showing the immune system has strong backup pathways.
Are some people born more vulnerable to infection?
Yes – but it depends on the situation.
-
Children with very low MBL may get more ear, chest, or sinus infections while their immune systems are developing.
-
In adults, MBL deficiency usually only matters if there are other risks, such as chronic lung disease, immune suppression, or another immune problem.
-
Many people with low MBL live their whole lives without extra infections.
MBL deficiency and aspergillosis
On its own, MBL deficiency rarely causes illness. But in people who already have other risks – such as lung disease (COPD, asthma, bronchiectasis, or TB damage) or a weakened immune system – it may make infections more likely.
Research suggests MBL deficiency can be linked to:
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Chronic pulmonary aspergillosis (CPA)
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Allergic bronchopulmonary aspergillosis (ABPA)
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Invasive aspergillosis in people with suppressed immunity
In these cases, MBL deficiency is not the single cause of aspergillosis, but it may be one of several factors that increase vulnerability.
Can MBL deficiency be treated?
At present, there is no routine treatment to replace MBL itself. Research has explored giving purified MBL, but it hasn’t become a standard therapy – largely because deficiency is so common and most people remain healthy without intervention.
Instead, management focuses on:
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Treating infections promptly with antibiotics or antifungals
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Sometimes using preventive (prophylactic) antibiotics or antifungals in people with frequent or severe infections
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Using immunoglobulin replacement therapy if there are additional immune problems
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Supporting lung health and reducing risks with vaccinations, good self-care, and specialist monitoring
Why measure MBL if it can’t be treated directly?
Even without a direct treatment, measuring MBL can still be useful:
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Helps explain recurrent infections – finding a low MBL level can give part of the reason why someone is more prone to infections.
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Part of a bigger immune work-up – it’s often checked alongside other immune tests, and the overall pattern may guide treatment decisions.
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Risk awareness – knowing about low MBL can make doctors more proactive with antibiotics, antifungals, or vaccinations, and encourage earlier treatment at the first sign of infection.
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Research value – helps specialists understand why some people develop aspergillosis while others don’t.
Why hasn’t evolution eliminated low MBL?
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Common worldwide: 5–10% of people have very little MBL, and up to 30% have reduced levels. If this were a major disadvantage, numbers would be lower.
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Other immune pathways compensate: The body has strong backup systems, so many people stay healthy even with low MBL.
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Possible advantage: In some infections, high MBL may drive too much inflammation. Lower MBL might have protected against diseases like leprosy or TB.
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Changing disease patterns: In the past, people rarely lived long enough for chronic lung disease to show the effects of low MBL. Today, with longer lives and modern medicine, its role is more visible.
👉 In short: low MBL has not been “selected out” by evolution because it usually isn’t harmful on its own, and in some situations it may even have been protective.
What this means for patients
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Having MBL deficiency is quite common and usually harmless.
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It may become more relevant if you also have underlying lung disease or are on treatments that suppress the immune system.
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If MBL deficiency is suspected, doctors may check for it as part of a wider immune work-up.
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The key point: treatment is aimed at managing infections and lung health, not the MBL level itself.
👉 In short: MBL deficiency is common in the general population. Most people never notice it, but for some with lung disease or weakened immunity, it may add to the risk of aspergillosis. While there’s no direct treatment for the deficiency, testing can help explain recurrent infections, guide wider immune checks, and shape preventive care.
NHS England - You and Your GP: Key Points for NHS Patients Managing Aspergillosis
You and your general practice (YYGP) has been developed to help patients understand what to expect from their general practice and how they can get the best from their GP team. YYGP also enables patient to provide feedback or raise concerns with their GP Practice, Healthwatch or the integrated care board. The contract requires every GP practice to have linked to the NHS England YYGP document on their website, no later than 1 October 2025.
1. Accessing Your GP
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Opening hours: Your GP is typically open 8:00 – 18:30, Monday to Friday. You can walk in, call, or use the NHS App or practice website to contact them NHS England.
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If closed: For urgent but non-emergency needs, use 111 online or by calling 111 NHS England.
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In an emergency: If symptoms are life-threatening (e.g., sudden severe breathing issues), go to A&E or call 999 NHS England.
2. Making an Appointment
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When you contact your GP—whether by phone, online, or in person—they’ll assess your condition and respond within one working day with next steps NHS England.
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This could include:
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A face-to-face appointment
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A phone consultation
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A text message with advice
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A recommendation to consult a pharmacy or another NHS service NHS England.
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This prompt response is especially important for aspergillosis fluctuations or side effects from antifungal treatments.
3. Who You'll See
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You may be seen by a GP, nurse, or pharmacist.
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If you have a designated carer, they can speak on your behalf (with your permission).
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If you prefer a specific healthcare professional you trust, request them—though waits might be longer NHS England.
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Seeing the same clinician regularly can be beneficial for managing complex, long-term conditions like aspergillosis NHS England.
4. Support for Additional Needs
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If English isn't your first language, you can request interpretation services when booking an appointment.
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If you need extra help—like longer appointments, a quiet space, wheelchair access, or materials in accessible formats—just let the practice know; they'll try to accommodate NHS England.
5. Changing or Selecting a GP
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You can find or switch to a GP using the NHS website (“Find a GP”) or by contacting local practices directly NHS England.
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No ID, NHS number, or proof of address is needed to register—even if you’re homeless or your immigration status is uncertain NHS England.
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If a practice cannot register you, they must explain their decision in writing within 14 days NHS England.
6. Referral and Treatment Flexibility
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If your GP refers you to a specialist (e.g., respiratory consultant), you often have the right to choose your hospital or clinic NHS England.
7. Free Care & Private Work
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GP services are free, including appointments and treatments.
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Extra services like insurance letters may incur a fee NHS England.
8. Being a Helpful Patient
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Prepare for appointments: list symptoms, treatment concerns, and questions in advance.
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Be punctual or cancel in good time to avoid delays for others.
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Use the NHS App or website to book appointments, refill prescriptions, and view test results.
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Turn on App notifications to stay updated with messages from your practice NHS England.
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Order repeat prescriptions well ahead—especially vital when managing antifungal medications—to avoid running out NHS England.
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Consider joining the Patient Participation Group at your practice to share feedback and help improve services NHS England.
9. Sharing Feedback or Concerns
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To raise concerns, talk to your practice manager first.
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If needed, you can escalate feedback to your local Integrated Care Board (ICB).
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You can also reach out to your local Healthwatch (an independent NHS watchdog) for confidential advice and support NHS England.
Why This Matters for Aspergillosis Patients
Aspergillosis often requires ongoing monitoring, regular breathing tests, imaging, and antifungal therapy adjustments. Timely access to GP services, continuity of care, and preparedness all enhance your ability to manage flare-ups or side effects effectively.
Handy Checklist (for easy reference)
| Task |
|---|
| Contact GP promptly for new or worsening symptoms |
| Prepare questions ahead—e.g., changes in breathing, treatment effects |
| Use NHS App to manage appointments and medications |
| Order repeat prescriptions early to maintain drug access |
| Request support services if needed (interpretation, accessibility) |
| Provide feedback to improve your experience and others' |
Damp, Cold, and Poor Housing – Why It Matters for Lung Health
This briefing from the House of Commons Library (2025) looks at how poor housing conditions—especially damp, mould, and cold homes—affect health and what’s being done about it in the UK.
Main Points
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Health risks are serious
Living in damp or mouldy homes increases the risk of respiratory problems, particularly for people with existing lung disease like aspergillosis, asthma, COPD, or bronchiectasis. -
Children and vulnerable adults
Young children, older adults, and people with weakened immune systems are most affected. Damp and mould can trigger flare-ups, worsen breathing symptoms, and increase infection risk. -
Mental health impact
Poor housing is linked to stress, anxiety, and depression. Worrying about your home can also worsen physical symptoms, especially if you avoid using rooms with mould or limit heating to save costs. -
Cold homes add to the problem
Cold airways can make breathing more difficult, weaken the immune system, and increase the chance of winter infections. -
Wider health effects
Damp and cold can also affect heart health, bone/joint pain, and overall wellbeing.
What’s Being Done
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Legal responsibilities: Landlords must keep homes safe and fit to live in under UK law. This includes dealing with serious damp and mould.
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Government programmes:
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Funding for improving insulation and heating in social housing.
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Advice services for tenants.
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Local councils can take action if landlords fail to address hazards.
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Public health guidance now recognises the link between housing and chronic illness, with stronger advice for early intervention.
What This Means for Aspergillosis Patients
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Stay alert to symptoms: If your cough, breathlessness, or fatigue worsen at home, check for damp, mould, or poor heating.
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Act early: Report problems to your landlord or council quickly—prolonged exposure can worsen lung damage.
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Medical link is recognised: You are more likely to be taken seriously now, as official guidance acknowledges the health risks.
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Keep records: Photos, symptom diaries, and GP notes can support housing complaints.
For full details see https://commonslibrary.parliament.uk/research-briefings/cdp-2025-0096/
📘 What is CPA? (Chronic Pulmonary Aspergillosis)
Patient handout for A&E staff who are not aware of aspergillosis.
What is CPA?
CPA is a chronic fungal infection of the lungs caused by Aspergillus, most often in people who already have damaged lungs from conditions like tuberculosis, COPD, lung cancer, or sarcoidosis.
Unlike ABPA, CPA is a true infection, not an allergic reaction. It is not contagious but can slowly destroy lung tissue if not treated.
Symptoms
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Chronic cough, often with mucus
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Coughing up blood (haemoptysis)
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Fatigue, low-grade fever
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Unexplained weight loss
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Breathlessness
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Recurrent chest infections not responding to antibiotics
Diagnosis
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CT scan of the chest showing cavities, nodules, or fungus balls (aspergillomas)
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Aspergillus IgG antibody (usually raised)
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Positive sputum PCR or culture for Aspergillus
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Exclude TB and malignancy
Treatment
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Long-term antifungal therapy (e.g. itraconazole, voriconazole, posaconazole)
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Monitor blood levels and liver function
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Surgery or embolisation if severe bleeding occurs
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Supportive care: oxygen, nutrition, physiotherapy
Key Points for A&E:
✅ CPA is a progressive fungal infection, not a typical bacterial pneumonia
✅ May present with haemoptysis, respiratory distress, or systemic illness
✅ Review current antifungal treatment and potential drug interactions
✅ Consider urgent chest CT and specialist referral if patient is unwell
📍 For specialist support:
National Aspergillosis Centre (NAC)
🏥 Wythenshawe Hospital, Manchester University NHS Foundation Trust
🌐 NAC homepage on MFT website https://mft.nhs.uk/wythenshawe/services/infectious-diseases/national-aspergillosis-centre/
🌐 www.aspergillosis.org
📞 Daytime contact: 0161 291 2891 or 0161 291 4362
📞 Urgent out-of-hours: Call Wythenshawe switchboard on 0161 998 7070
📢 Ask for the on-call Infectious Diseases Consultant
📘 What is ABPA? (Allergic Bronchopulmonary Aspergillosis)
Patient handout for A&E staff who ask what aspergillosis is.
What is ABPA?
ABPA is an allergic lung condition caused by the immune system overreacting to the fungus Aspergillus. It mainly affects people with asthma or cystic fibrosis.
When Aspergillus spores are inhaled, most people clear them without issue. In ABPA, the immune system sees these spores as dangerous and mounts a strong inflammatory response. This leads to asthma-like symptoms, mucus plugging, and can result in permanent lung damage (bronchiectasis) if left untreated.
Symptoms
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Worsening breathlessness
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Wheezing, chest tightness
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Coughing up thick, often brown mucus
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Fever, fatigue, or feeling generally unwell
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Unintentional weight loss (advanced cases)
Diagnosis
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History of asthma or cystic fibrosis
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High IgE levels and positive Aspergillus-specific IgE
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Eosinophilia (raised white blood cells)
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Sputum culture or PCR positive for Aspergillus
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Chest imaging showing mucus plugging or bronchiectasis
Treatment
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Oral corticosteroids (e.g. prednisolone) to reduce inflammation
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Antifungal medication (e.g. itraconazole) to lower fungal burden
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Biologic therapies (e.g. omalizumab or benralizumab) in some patients
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Regular monitoring by respiratory or infectious diseases specialists
Key Points for A&E:
✅ ABPA is an allergic lung disease, not a classical infection
✅ Can present with severe asthma, mucus plugging, or type 2 respiratory failure
✅ Requires early recognition and often systemic steroids and antifungal therapy
✅ Take bloods (IgE, eosinophils, CRP), consider chest imaging, and review oxygen status
📍 For specialist support:
National Aspergillosis Centre (NAC)
🏥 Wythenshawe Hospital, Manchester University NHS Foundation Trust
🌐 NAC homepage on MFT website https://mft.nhs.uk/wythenshawe/services/infectious-diseases/national-aspergillosis-centre/
🌐 www.aspergillosis.org
📞 Daytime contact: 0161 291 2891 or 0161 291 4362
📞 Urgent out-of-hours: Call Wythenshawe switchboard on 0161 998 7070
📢 Ask for the on-call Infectious Diseases Consultant









