NHS:10 year plan

The NHS Long Term Plan, published in January 2019, outlines a comprehensive strategy to transform the NHS in England over the next decade. It aims to improve patient care, enhance efficiency, and ensure the sustainability of the health service. The plan focuses on several key areas: 

🏥 1. A New Service Model for the 21st Century

  • Integrated Care Systems (ICSs): Establishing ICSs across England to coordinate services and improve population health. 

  • Community-Based Care: Shifting focus from hospital-centric care to community and primary care, providing services closer to patients' homes.

  • Digital Access: Expanding digital services, including online consultations and access to health records, to enhance patient convenience.

🩺 2. Preventing Illness and Tackling Health Inequalities

  • Preventive Measures: Implementing programs to reduce smoking, obesity, and alcohol-related harm. 

  • Early Detection: Enhancing screening and early diagnosis for conditions like cancer and cardiovascular diseases.

  • Addressing Disparities: Focusing on reducing health inequalities across different communities.

🧠 3. Improving Mental Health Services

  • Increased Funding: Allocating additional resources to mental health services.

  • Access Expansion: Improving access to mental health support for children, adolescents, and adults.

  • Crisis Care: Developing comprehensive crisis care services available 24/7.

👶 4. Supporting Children and Maternity Services

  • Maternity Care: Enhancing continuity of care during pregnancy and childbirth.

  • Child Health: Improving services for children with complex needs and expanding immunisation programs.

🧬 5. Advancing Genomic and Personalised Medicine

  • Genomic Testing: Integrating genomic testing into routine care to personalise treatment plans.

  • Research and Innovation: Investing in research to develop new treatments and technologies.

💻 6. Embracing Digital Technology

  • Electronic Health Records: Ensuring all patient records are digitized and accessible across care settings.

  • Telehealth Services: Expanding virtual consultations and remote monitoring to increase access and efficiency.

👩‍⚕️ 7. Workforce Development

  • Staff Recruitment and Retention: Implementing strategies to attract and retain healthcare professionals.

  • Training and Education: Providing continuous professional development opportunities for NHS staff.

💷 8. Financial Sustainability

  • Efficient Resource Use: Reducing administrative costs and reinvesting savings into patient care.

  • Funding Allocation: Ensuring funds are directed towards areas with the greatest impact on health outcomes.

The NHS Long Term Plan represents a significant commitment to transforming healthcare delivery in England, focusing on prevention, personalisation, and integration to meet the evolving needs of the population.

For more detailed information, you can access the full plan here: NHS Long Term Plan.

by GAtherton

Your NHS

The structure of the NHS (National Health Service)—particularly in the UK context—helps promote community, integrity, moral values, and ethics in several ways. While the NHS is often under pressure, its core design remains rooted in collective responsibility, public service ethics, and social solidarity.

🧭 1. Foundational Principles Reflect Ethical Commitments

The NHS was founded in 1948 on three core principles:

  • It meets the needs of everyone

  • It is free at the point of delivery

  • It is based on clinical need, not ability to pay

These principles are inherently moral—they prioritise fairness, compassion, and equal dignity, reinforcing the value that health care is a public good, not a commodity.

🏘️ 2. Community-Centred Service Delivery

  • Local NHS trusts and Integrated Care Systems (ICSs) deliver care close to where people live. This local structure:

    • Encourages community engagement

    • Supports collaboration with charities, social care, and volunteers

    • Reflects local health needs and inequalities

This fosters a sense of shared ownership, where patients and clinicians work within and for their communities.

🩺 3. Professional Integrity and Ethical Training

  • NHS staff are bound by strict professional codes of conduct (e.g. GMC, NMC) promoting:

    • Honesty, accountability, respect, and patient autonomy

  • Ethical frameworks guide decision-making in:

    • Consent

    • End-of-life care

    • Resource prioritisation

Training and reflective practice help staff embed moral reasoning in everyday clinical work.

🤝 4. Public Service Ethos and Social Trust

Because NHS workers are public servants, not driven by profit, the service promotes:

  • A duty to care over personal gain

  • Greater transparency and scrutiny

  • Stronger patient trust

Polling consistently shows that the public views NHS staff as among the most trusted professions in the UK.

💷 5. Universal Funding Model

  • Funded largely through progressive taxation, the NHS embodies solidarity—the healthy contribute to the sick, the wealthy to the less well-off.

  • This builds a shared sense of mutual support, unlike systems that divide people by insurance status or income.

📣 6. Ethical Frameworks for Difficult Choices

When resources are limited (e.g., organ transplants, ICU beds), the NHS applies publicly debated ethical frameworks:

  • NICE decisions are based on cost-effectiveness and fairness

  • Pandemic response planning includes ethics boards and public input

This helps maintain moral legitimacy even in hard decisions.

🚨 Challenges and Reality Check

While the NHS structure supports ethics and community, underfunding, waiting lists, and workforce shortages sometimes strain these ideals. However, the institutional values remain intact, and many staff stay in the NHS because of these shared values.

🌱 In Summary

The NHS promotes community, integrity, and ethics through:

  • Universal access based on need

  • Local, community-led care

  • Public funding and service ethos

  • Professional ethical codes

  • Fair, transparent decision-making

It is not just a healthcare system—it’s a moral statement about what a society owes its people.

by GAtherton

🌿 Tezepelumab (Tezspire) and ABPA: What You Need to Know

If you’ve been living with ABPA and find your symptoms keep coming back despite steroids and antifungal treatment, your consultant may suggest a biologic (monoclonal antibody). One of the newer options being offered to some patients in the UK is Tezepelumab, brand name Tezspire.

💡 What is Tezepelumab?

Tezepelumab is a biologic injection that targets a molecule called TSLP (thymic stromal lymphopoietin). TSLP is an early trigger in the chain reaction that leads to inflammation in the lungs. By blocking it, Tezepelumab can calm multiple allergic and eosinophilic pathways, which makes it different from most other biologics that only block one type of inflammation.

✅ Who Might Be Offered Tezepelumab?

Tezepelumab is approved by NICE for use in the NHS in people aged 12+ with severe asthma, especially those who:

  • Are on high-dose inhaled steroids and still struggling

  • Have had 3+ asthma flare-ups in the last year, or

  • Need to take regular oral steroids

If you have both ABPA and severe asthma, you might be offered Tezepelumab—even though it isn’t specifically licensed for ABPA.

🔍 How Does It Compare to Other Biologics?

Here’s a quick comparison:

Biologic Name Target NHS Use Needs High IgE or Eosinophils?
Omalizumab IgE Severe allergic asthma ✅ Yes – High IgE needed
Mepolizumab IL-5 Eosinophilic asthma ✅ Yes – High eosinophils needed
Benralizumab IL-5 receptor Eosinophilic asthma ✅ Yes
Dupilumab IL-4/13 Allergic asthma ❌ No, but usually allergy-type
Tezepelumab TSLP (upstream) Severe asthma (NICE-approved) ❌ No – works across all types

🧠 Why this matters: If your IgE or eosinophil levels aren’t high, Tezepelumab may still work for you—even when other biologics aren't suitable.

💷 Is Tezepelumab Expensive?

Yes—but it's funded on the NHS for patients who meet NICE criteria.

  • List price: ~£1,265 per injection (monthly)

  • NHS pays less through a confidential discount agreement

  • It’s not necessarily cheaper than other biologics, but it offers wider eligibility and broad activity

⚖️ Is It Better Than Other Biologics?

It depends. Some patients respond well to older biologics like omalizumab or mepolizumab, especially if their ABPA overlaps with allergy or eosinophilic asthma. But Tezepelumab may be a better fit if:

  • You don’t qualify for the others (e.g. your IgE is too low)

  • You’ve tried other biologics and they didn’t help enough

  • Your ABPA overlaps with hard-to-control asthma

While Tezepelumab isn’t licensed specifically for ABPA, its upstream targeting may help reduce flare-ups in those with overlapping conditions.

💉 Side Effects

Most people tolerate Tezepelumab well. Possible side effects include:

  • Injection site reactions (redness, swelling)

  • Headache or sore throat

  • Allergic reaction (rare)

It's given by subcutaneous injection once a month, often at hospital initially, but home administration may be an option later on.

👩‍⚕️ What to Ask Your Consultant

  • Why are you recommending this biologic for me?

  • Will it help with both my ABPA and asthma?

  • How soon should I expect results?

  • Can I stop steroids if this works?

Keeping a symptom diary and reporting back is really useful to your team.

🧾 Summary

Question Tezepelumab (Tezspire) Answer
Licensed for ABPA? ❌ No, but used off-label when asthma overlaps
Approved for NHS use? ✅ Yes – via NICE for severe asthma
IgE or eosinophils needed? ❌ No
Dose/frequency Monthly injection
Broad anti-inflammatory effect? ✅ Yes – acts early in the pathway

Tezepelumab is opening new doors for people with ABPA and severe asthma who’ve struggled with flare-ups, steroid side effects, or biologics that didn’t work. It’s not for everyone, but it’s worth a conversation with your specialist.

by GAtherton

🧬 Biologic Treatments for ABPA (Allergic Bronchopulmonary Aspergillosis)

Many people with ABPA who continue to experience flare-ups despite steroids and antifungals are now being offered biological therapies—also known as monoclonal antibodies.

These treatments target specific parts of the immune system involved in allergic inflammation. They're often used when:

  • Steroids are needed frequently or at high doses

  • Antifungals alone aren’t enough

  • ABPA keeps recurring and affecting quality of life

💉 Biologics Currently Used in ABPA

The following biologics are being used in the UK, particularly in specialist centres and often in patients with ABPA plus severe asthma or eosinophilic disease:

Biologic Name Target Brand Name Notes
Omalizumab IgE Xolair Most commonly used; good for high IgE and allergic asthma
Mepolizumab IL-5 Nucala For eosinophilic inflammation; steroid-sparing
Benralizumab IL-5 receptor (IL-5Rα) Fasenra Rapidly reduces eosinophils; monthly or 8-weekly injection
Dupilumab IL-4 and IL-13 Dupixent Used in allergic-type asthma and some ABPA patients
Reslizumab IL-5 Cinqaero IV infusion; less commonly used in ABPA
Tezepelumab TSLP (upstream cytokine) Tezspire Newest option; blocks multiple inflammatory pathways; doesn’t require high IgE or eosinophils

👉 Note: No biologic is officially licensed specifically for ABPA, but many are used off-label in patients with overlapping severe asthma or allergic disease.

✅ What Do Patients Say?

Many people treated with biologics report:

  • Fewer flare-ups or “chest infections”

  • Less need for oral steroids

  • Clearer breathing, less coughing, and better energy

Not everyone responds, but many see significant improvement in control and quality of life.

⚠️ Side Effects

Biologics are generally well-tolerated. Possible side effects include:

  • Mild injection site reactions (redness, swelling)

  • Headaches or fatigue

  • Allergic reactions (rare)

They’re usually given every 2–8 weeks as an injection under the skin, sometimes in hospital at first and then possibly at home.

🩺 What to Ask Your Consultant

  • Why have you chosen this biologic for me?

  • Will it help my asthma as well as ABPA?

  • How soon will I know if it’s working?

  • Will I still need antifungals or steroids?

  • Are there any alternatives if this one doesn’t work?

📌 Summary

Key Point Biologics in ABPA
Used when Steroids aren’t enough or cause side effects
Most used Omalizumab, Mepolizumab, Tezepelumab
Goals Reduce flares, improve breathing, lower steroid use
Licensed for ABPA? ❌ No – but used off-label in many UK centres
NHS funding? ✅ Yes – when criteria for severe asthma are met

by GAtherton

Understanding Aspergillosis: A Guide for Expert Patients and Clinical Professionals

Aspergillosis is an umbrella term for a group of diseases caused by infection or hypersensitivity to fungi in the Aspergillus genus, most commonly Aspergillus fumigatus. The spectrum of disease ranges from benign colonisation to aggressive, life-threatening invasive infection, depending on the host’s immune status and pre-existing lung condition.

🔍 Main Forms of Aspergillosis

Type Description Typical Host
Allergic Bronchopulmonary Aspergillosis (ABPA) A hypersensitivity reaction to A. fumigatus in the airways, with airway inflammation and mucus plugging Asthma or cystic fibrosis patients
Chronic Pulmonary Aspergillosis (CPA) Long-term infection of damaged lung tissue; may form cavities, fibrosis, or fungal balls (aspergilloma) Patients with COPD, TB history, sarcoidosis, or bronchiectasis
Aspergilloma A fungal ball within a lung cavity, often seen in CPA Pre-existing lung cavity from TB or sarcoidosis
Invasive Aspergillosis (IA) Rapid tissue-invasive fungal infection, often bloodstream dissemination Immunocompromised hosts (neutropenia, transplant, high-dose steroids, haematological malignancy)
Sinopulmonary and Disseminated Aspergillosis Involvement of sinuses, CNS, bone, or multiple organs Usually in immunocompromised or advanced disease
Allergic Aspergillus Sinusitis (AAS) Similar to ABPA but in the sinuses Atopic individuals, often with nasal polyposis

👥 Who Is Vulnerable?

Risk varies by form:

1. ABPA

  • Adults or children with moderate-to-severe asthma

  • Patients with cystic fibrosis

2. CPA / Aspergilloma

  • Structural lung disease: TB scarring, COPD, sarcoidosis, bronchiectasis

  • Immune dysregulation: diabetes, corticosteroid use

3. Invasive Aspergillosis

  • Neutropenic patients (especially haematological malignancies)

  • Solid organ or stem cell transplant recipients

  • Chronic granulomatous disease

  • ICU patients (especially with influenza or COVID-19)

⚠️ Main Symptoms and Diagnostic Red Flags

Symptom Suggestive Of
Persistent cough, often productive ABPA or CPA
Wheeze, breathlessness, chest tightness ABPA
Haemoptysis (mild to severe) Aspergilloma, CPA, sometimes ABPA
Weight loss, fatigue, night sweats CPA or IA
Facial pain, nasal discharge Aspergillus sinusitis
Fever, hypoxia, sepsis signs Invasive aspergillosis

🧪 Diagnosis

📌 ABPA

  • Elevated total IgE (>1000 IU/mL)

  • Raised Aspergillus-specific IgE/IgG

  • Eosinophilia

  • Chest CT: central bronchiectasis, mucus impaction ("finger-in-glove")

  • Positive sputum culture or PCR for A. fumigatus

📌 CPA

  • Symptoms >3 months

  • Chest imaging: cavitary lesions, fungal ball, pleural thickening

  • Positive Aspergillus IgG

  • Repeated positive cultures/PCR from sputum or BAL

  • Exclusion of TB and other mimics

📌 Invasive Aspergillosis

  • Imaging: halo sign, air crescent sign on CT

  • Serum galactomannan, (1→3)-β-D-glucan, PCR

  • BAL galactomannan and culture

  • Tissue biopsy (definitive)

💊 Treatment Approaches

🟦 ABPA

  • Oral corticosteroids (mainstay)

  • Itraconazole or posaconazole to reduce fungal burden

  • Biologics (e.g. omalizumab, mepolizumab, benralizumab) in steroid-dependent or resistant cases

🟧 CPA

  • Long-term triazole antifungals (e.g. itraconazole, voriconazole, posaconazole)

  • Monitoring of serum drug levels, liver function

  • Surgical resection in selected cases (aspergilloma)

  • Inhaled amphotericin B in refractory cases

🟥 Invasive Aspergillosis

  • Voriconazole (first-line)

  • Liposomal amphotericin B (alternative)

  • Duration: typically 6–12 weeks

  • Manage immunosuppression, treat underlying disease

🧭 Monitoring and Follow-up

  • Serial imaging (CT or X-ray)

  • Aspergillus IgG/IgE titers

  • Liver function and antifungal serum levels

  • Patient-reported symptom scores and quality of life

📚 Further Information and Resources

  • National Aspergillosis Centre (NAC): aspergillosis.org,

  • UK Clinical Guidelines: BTS CPA Guidelines (2016), ERS ABPA position paper (2020)

  • Support Groups: NAC Patient Support Facebook Group, Aspergillosis Trust

  • Referral Pathway: Respiratory teams can refer to NAC via NHS e-Referral system or Advice & Guidance. NAC is a tertiary NHS service so referrals cannot be made by a GP.

by GAtherton

COVID-19 Associated Pulmonary Aspergillosis (CAPA) for Expert Patients and non-Specialist Clinicians

Expert Information for Patients, GPs, and Specialist Nurses

🔎 What Is CAPA?

CAPA is a form of invasive pulmonary aspergillosis (IPA) that develops in patients with severe COVID-19, particularly those in intensive care units (ICU) with acute respiratory distress syndrome (ARDS). It is an opportunistic fungal infection caused by Aspergillus fumigatus, occurring without traditional risk factors such as neutropenia.

CAPA is part of the broader group of IAPA (Influenza-Associated Pulmonary Aspergillosis) and VAPA (Viral-Associated Pulmonary Aspergillosis).

🧬 Pathophysiology

  • Severe viral pneumonia (COVID-19) damages the airway epithelium.

  • Inhaled Aspergillus spores invade damaged lung tissue.

  • Corticosteroids (e.g. dexamethasone), immunomodulators (e.g. tocilizumab), and prolonged ventilation increase susceptibility.

👥 Who Is at Risk?

Primarily affects patients with:

  • Severe COVID-19 pneumonia, especially those with:

    • ICU admission

    • Mechanical ventilation

    • ARDS

  • Corticosteroid therapy or IL-6 inhibitors (e.g. tocilizumab)

  • Underlying lung disease (COPD, asthma)

  • Diabetes mellitus

📍 CAPA may occur even in immunocompetent individuals due to local lung immune disruption.

⚠️ Clinical Features

Often non-specific and difficult to distinguish from worsening COVID-19:

  • Persistent or worsening respiratory failure

  • New pulmonary infiltrates on imaging

  • Fever despite antibacterial therapy

  • Haemoptysis or pleuritic chest pain (less common)

  • Increased oxygen or ventilatory support requirement

🧪 Diagnosis

CAPA is challenging to diagnose and relies on clinical suspicion, radiology, and mycological evidence.

Diagnostic Tools:

  • CT Chest:

    • Nodules, cavitations, halo sign (often non-specific in COVID)

  • Bronchoscopy with BAL:

    • Galactomannan (BAL GM ≥1.0 = probable CAPA)

    • Culture and PCR for Aspergillus

  • Serum Galactomannan or β-D-glucan:

    • May be positive but less sensitive than BAL

  • Histopathology (rarely obtained due to ICU setting)

Diagnostic Categories (ECMM/ISHAM 2020):

  • Proven: histology showing fungal invasion

  • Probable: radiology + mycology from BAL

  • Possible: suggestive clinical picture + limited microbiology

💊 Treatment

First-Line:

  • Voriconazole (IV or oral)

  • Isavuconazole (alternative with fewer side effects)

  • Consider liposomal amphotericin B if azole resistance or intolerance

Additional Considerations:

  • Therapeutic drug monitoring (TDM) required for voriconazole

  • Duration: typically 6–12 weeks depending on response and immune status

  • Minimise immunosuppression where possible

Empirical antifungal therapy may be started in ICU when suspicion is high, even before full confirmation.

🧾 Monitoring

  • Respiratory function

  • Repeat imaging to assess progression or resolution

  • Serum galactomannan

  • Liver function, renal function, and drug levels

  • Screen for drug interactions (especially with azoles)

📚 More Information

  • CAPA is a recently recognised entity, requiring close coordination between ICU, respiratory, and infectious disease teams.

  • Early antifungal treatment improves outcomes, but diagnosis is often delayed due to overlapping features with COVID-19 pneumonia.

  • Resources: ECMM/ISHAM CAPA definitions, aspergillosis.org

by GAtherton

Severe Asthma with Fungal Sensitisation (SAFS) for Expert Patients and non-Specialist Clinicians

Expert Information for Patients, GPs, and Specialist Nurses

🔎 What Is SAFS?

SAFS describes a clinical subgroup of patients with severe asthma who are sensitised to environmental fungi, particularly Aspergillus fumigatus, but who do not meet criteria for ABPA (i.e. no high total IgE or central bronchiectasis).

Fungal sensitisation may contribute to poor asthma control, airway inflammation, and increased exacerbations.

🧬 Pathophysiology

  • IgE-mediated sensitisation to fungi in the airways

  • Chronic airway inflammation exacerbated by fungal allergens

  • Unlike ABPA, no eosinophilia, mucus plugging, or significant IgE rise

👥 Who Is at Risk?

SAFS affects adults or children with:

  • Severe asthma (high-dose ICS + additional controller medication)

  • Recurrent exacerbations or persistent symptoms

  • Evidence of IgE sensitisation to fungi, especially A. fumigatus, Alternaria, Cladosporium

It may overlap with ABPA, and some patients may transition between the two.

⚠️ Common Symptoms

  • Poor asthma control despite optimal treatment

  • Frequent exacerbations

  • Airflow limitation (FEV1 often <80%)

  • Increased oral corticosteroid use

  • Wheeze, cough, chest tightness

🧪 Diagnosis

SAFS is a diagnosis of exclusion in patients with severe asthma and fungal sensitisation, but without ABPA.

Required Features:

  1. Severe asthma, typically on BTS Step 4–5 therapy

  2. Positive fungal-specific IgE (skin prick or blood) to at least one fungus

    • Aspergillus fumigatus most common

  3. No ABPA: i.e., total IgE <1000 IU/mL, no eosinophilia, no central bronchiectasis

Investigations:

  • Skin prick testing or specific IgE blood test

  • Total IgE to exclude ABPA

  • CT chest to rule out ABPA or CPA

  • Sputum culture for A. fumigatus (not required for diagnosis)

💊 Treatment

Antifungal Therapy:

  • Itraconazole (first-line): 3–6 months may improve asthma control, reduce exacerbations

  • Posaconazole (alternative)

  • Liver function and drug levels must be monitored

The EVITA 3 and Fungal Asthma trials suggest modest benefit with antifungal therapy in SAFS.

Asthma Management:

  • High-dose inhaled corticosteroids + LABA

  • Leukotriene receptor antagonists

  • Macrolides in selected patients (anti-inflammatory benefit)

  • Biologics:

    • Omalizumab (anti-IgE)

    • Mepolizumab, Benralizumab (anti-IL-5)

    • Dupilumab (anti-IL-4/13)

🧾 Monitoring

  • Asthma control questionnaires (ACT, ACQ)

  • Exacerbation frequency

  • Spirometry

  • Fungal IgE titres (do not typically change with treatment)

  • LFTs and drug levels if on antifungals

📚 More Information

  • SAFS patients often benefit from review in a specialist asthma clinic or severe asthma network centre.

  • Overlap with ABPA: patients should be periodically reassessed to detect transition to ABPA.

  • Patient resources: aspergillosis.org, Asthma + Lung UK, BTS asthma guidelines

  • Resource: SAFS

by GAtherton

Allergic Bronchopulmonary Aspergillosis (ABPA) for Expert Patients and non-Specialist Clinicians

Expert Information for Patients, GPs, and Specialist Nurses

🔎 What Is ABPA?

ABPA is a complex hypersensitivity reaction to Aspergillus fumigatus colonising the airways. It is not a fungal infection in the classic sense, but rather an exaggerated immune response — particularly involving IgE and eosinophils — seen in people with asthma or cystic fibrosis (CF).

It leads to recurrent inflammation, mucus plugging, and bronchial damage (including central bronchiectasis) if untreated.

🧬 Disease Mechanism

  • Type I and III hypersensitivity to A. fumigatus

  • Chronic airway inflammation causes mucus impaction and permanent lung damage

  • Associated with elevated total and specific IgE, eosinophilia, and recurrent flares

👥 Who Is at Risk?

  • Moderate to severe asthma

  • Cystic fibrosis

  • Rarely, patients with bronchiectasis or other chronic airway disease

ABPA is often underdiagnosed, especially in adults with difficult-to-control asthma.

⚠️ Common Symptoms

  • Worsening asthma control

  • Wheeze and chest tightness

  • Cough with thick mucus plugs

  • Shortness of breath

  • Intermittent low-grade fever

  • Haemoptysis (less common, usually mild)

  • Fatigue and poor response to inhaled steroids alone

🧪 Diagnosis

Diagnosis is based on a combination of clinical, radiological, and immunological features.

Core Investigations:

  1. Total IgE ≥1000 IU/mL (or >500 in treated patients)

  2. Aspergillus-specific IgE positive

  3. Aspergillus-specific IgG (or precipitating antibodies)

  4. Blood eosinophilia (>0.5 x10⁹/L typically)

  5. Chest CT: central bronchiectasis, mucus plugging (“finger-in-glove”), fleeting infiltrates

  6. Sputum culture or PCR positive for A. fumigatus

Diagnostic Criteria:

Use updated ISHAM criteria (2024 version preferred) combining major and minor features.

💊 Treatment

First-Line:

  • Oral corticosteroids (e.g. prednisolone) – cornerstone of flare management

    • Typically tapered over 3–6 months

Adjunct:

  • Itraconazole or posaconazole – reduces antigen burden and steroid need

    • 3–6 months or longer; monitor liver function and drug levels

Steroid-Sparing Options:

  • Biologics (increasingly used, especially in steroid-dependent or relapsing patients):

    • Omalizumab (anti-IgE)

    • Mepolizumab, Benralizumab (anti-IL-5)

    • Dupilumab, Tezepelumab (emerging options)

🧾 Monitoring

  • Total IgE every 1–3 months (a 25–50% rise may indicate relapse)

  • Pulmonary function tests (FEV1, peak flow)

  • Repeat CT if clinical deterioration or poor steroid response

  • Sputum cultures in persistent symptoms (to exclude Aspergillus bronchitis)

⚠️ Complications

  • Progression to bronchiectasis

  • CPA (if antifungals are stopped prematurely in chronic cases)

  • Recurrent flares leading to irreversible damage

  • Steroid side effects (weight gain, osteoporosis, adrenal suppression)

📚 More Information

  • Specialist referral: patients should be considered for referral to the National Aspergillosis Centre (NAC) or local respiratory immunology team for persistent/recurrent ABPA.

  • Patient support: aspergillosis.org, CF Trust, Asthma + Lung UK

  • Key guidelines: Guidance

by GAtherton

Aspergillus Tracheobronchitis (ATB) for Expert patients and non-Specialist Clinicians

Expert Information for Patients, GPs, and Specialist Nurses

🔎 What Is Aspergillus Tracheobronchitis?

Aspergillus tracheobronchitis (ATB) is a rare but serious form of airway-invasive aspergillosis that primarily affects the trachea and large bronchi, rather than the lung parenchyma. It occurs predominantly in immunocompromised patients and may present with obstructive airway symptoms or respiratory failure.

ATB can exist on a spectrum from superficial colonisation to ulcerative or pseudomembranous invasion of the bronchial wall.

🧬 Pathophysiology

  • Inhaled Aspergillus spores adhere to and invade damaged airway mucosa.

  • Occurs more commonly when local airway immunity is impaired (e.g. in transplant recipients or critical illness).

  • May co-exist with invasive pulmonary aspergillosis (IPA) or appear in isolation.

👥 Who Is at Risk?

High-risk groups include:

  • Lung transplant recipients

  • Hematopoietic stem cell transplant patients

  • Severe COPD or structural airway disease

  • Patients with prolonged corticosteroid use

  • Critically ill or mechanically ventilated patients

  • COVID-19 or influenza patients (sometimes overlapping with CAPA/IAPA)

⚠️ Clinical Presentation

Symptoms depend on the degree of airway obstruction and depth of invasion:

  • Cough (dry or productive)

  • Worsening breathlessness

  • Stridor or wheeze

  • Hoarseness or vocal changes

  • Fever unresponsive to antibiotics

  • Haemoptysis (may be life-threatening)

  • Airway obstruction or collapse in advanced cases

ATB may be mistaken for tracheobronchial malignancy, infection, or stenosis.

🧪 Diagnosis

Bronchoscopy is essential for diagnosis:

  • Direct visualisation of:

    • Ulceration

    • Pseudomembranes

    • Plaques

    • Necrotic debris

  • Biopsies may reveal fungal hyphae invading mucosa.

Microbiological Investigations:

  • Culture and PCR for Aspergillus from BAL or brushings

  • BAL galactomannan

  • Serum galactomannan or β-D-glucan may be supportive

  • CT chest may be normal or show airway thickening, bronchial wall invasion, or tree-in-bud opacities

💊 Treatment

Systemic Antifungals:

  • Voriconazole is first-line

  • Isavuconazole or liposomal amphotericin B if azole intolerant or resistant

Airway Management:

  • Debridement or bronchoscopic removal of pseudomembranes in severe obstruction

  • Airway stenting in refractory strictures

  • Nebulised antifungals (e.g. amphotericin B) may be used as adjunct in selected cases

Prompt initiation of antifungal therapy is vital. Delays can lead to respiratory failure or death.

🧾 Monitoring

  • Clinical response: breathlessness, cough, fever

  • Repeat bronchoscopy in some cases

  • CT imaging of airways

  • Antifungal drug levels

  • Liver and renal function

📚 More Information

  • ATB is under-recognised, especially in non-neutropenic or critically ill patients.

  • Should be considered in transplant recipients or ICU patients with persistent respiratory symptoms and negative bacterial cultures.

  • Referral to respiratory, infectious diseases, and ICU teams is essential.

  • Resources: aspergillosis.org ; BTS Statement on  aspergillosis

by GAtherton

Aspergillus Bronchitis for Expert Patients and non-Specialist Clinicians

Expert Information for Patients, GPs, and Specialist Nurses

🔎 What Is Aspergillus Bronchitis?

Aspergillus bronchitis is a chronic fungal infection of the airways by Aspergillus fumigatus (or rarely other Aspergillus species), seen in individuals with structural lung disease or impaired mucociliary clearance. Unlike ABPA, it is not allergic in origin and does not involve systemic invasion, but is characterised by persistent fungal colonisation with active infection.

🧬 Pathophysiology

  • Chronic colonisation of the conducting airways by Aspergillus

  • Local immune dysfunction (but not systemic immunosuppression)

  • Low-grade inflammation and increased mucus production

  • Often coexists with bronchiectasis, COPD, or CF

👥 Who Is at Risk?

Most commonly seen in patients with:

  • Bronchiectasis (non-ABPA)

  • Cystic fibrosis

  • COPD or asthma with sputum production

  • Post-viral or structural airway damage

  • Chronic antibiotic or corticosteroid use

Not typically seen in severely immunocompromised hosts (in whom invasive aspergillosis is more likely).

⚠️ Common Symptoms

  • Persistent productive cough

  • Thick sputum often yellow or green

  • Worsening breathlessness or wheeze

  • Chronic sputum positivity for Aspergillus

  • Mild fever or malaise (but often afebrile)

  • Poor response to antibiotics alone

Symptoms may resemble chronic bacterial bronchitis or overlap with infective exacerbations of bronchiectasis.

🧪 Diagnosis

Diagnosis requires a combination of clinical and microbiological evidence, with exclusion of ABPA and CPA.

Diagnostic Features:

  1. Chronic productive cough (>4 weeks)

  2. Repeated isolation of Aspergillus from sputum or BAL

  3. Elevated Aspergillus IgG (typically present)

  4. Normal or mildly elevated total IgE (typically <1000 IU/mL)

  5. Absence of cavitary lesions or ABPA features on CT

  6. Response to antifungal treatment supports diagnosis

🛑 Exclude:

  • ABPA (IgE >1000, eosinophilia, central bronchiectasis)

  • CPA (cavities, weight loss, radiological progression)

💊 Treatment

First-Line:

  • Oral antifungals (usually for 3–6 months)

    • Itraconazole (first choice)

    • Voriconazole or posaconazole (if resistant/intolerant)

  • Monitor drug levels and LFTs

Adjuncts:

  • Physiotherapy and airway clearance techniques

  • Nebulised saline or mucolytics

  • Treat co-infections (e.g. Pseudomonas) where relevant

In patients with CF, consider co-management with a specialist CF team.

🧾 Monitoring

  • Sputum cultures to monitor persistence or clearance

  • Aspergillus IgG levels

  • Symptoms (sputum, breathlessness)

  • Liver function and drug monitoring

  • Periodic CT imaging if symptoms worsen or haemoptysis occurs

📚 More Information

by GAtherton