🏥 Can a GP Refer You Directly to the National Aspergillosis Centre (UK)?

Unfortunately, no — not directly.

The NAC is a tertiary referral centre, meaning that:

  • Referrals must come from a hospital consultant (usually a respiratory or infectious diseases specialist)

  • The NAC cannot accept direct referrals from GPs or from patients themselves

This is due to NHS policy and service structure — not because they don’t want to help.


What Your GP Can Do:

Even though they can’t refer you directly, your GP can advocate on your behalf and help move things forward by:

  1. Writing to your current hospital consultant to request:

    • A second opinion from NAC

    • Transfer of care or joint management with NAC

    • Review of your images, sputum results, and previous history

  2. If your current hospital won’t cooperate, your GP can:

    • Refer you to a different respiratory consultant (at another hospital if needed)

    • Ask that this new consultant considers NAC referral

  3. If your case involves rare, persistent, or poorly controlled lung disease with suspected Aspergillus involvement, the NAC is usually happy to review — but only after that consultant request is made.


📂 What to Send (via the consultant)

Your hospital team (at your GP’s request) should ideally send:

  • Latest CT scans and chest X-rays

  • Sputum culture results

  • Total and specific IgE / Aspergillus IgG

  • A clear clinical history summary

  • Any previous diagnosis letters or clinic notes


🗣️ If You’re Still Not Getting Help

If your current consultants won’t help and your GP is willing, you might also:

  • Ask your GP to refer you to a private respiratory specialist (for one appointment only) who may agree to refer you to NAC from there.

  • Or contact your local Patient Advice and Liaison Service (PALS) to escalate the block in access.


💬 Suggested Wording for Your GP:

“I’ve had long-standing respiratory symptoms with suspected Aspergillus involvement and limited progress under my current hospital team. I understand referral to the National Aspergillosis Centre requires a hospital consultant, but would you be willing to request that my current team (or an alternative respiratory consultant) considers this referral on my behalf?”


💡 Summary:

  • ❌ GPs cannot refer you directly to NAC

  • ✅ Your GP can request your hospital consultant do it — and advocate for you

  • 🛑 If you're being blocked, ask to be referred to another consultant who may be more open to referring to NAC


🌬️ Understanding the FeNO Test: What It Means for People with Asthma or ABPA

If you’ve been diagnosed with asthma or ABPA (Allergic Bronchopulmonary Aspergillosis), your healthcare team may use a test called FeNO to help assess your condition. But what exactly is FeNO — and what does it tell us?

Let’s break it down in simple terms.


✅ What Is FeNO?

FeNO stands for "Fractional exhaled Nitric Oxide." It’s a simple breathing test that measures how much nitric oxide gas you breathe out.

Why is this important? Because nitric oxide levels in your breath are linked to inflammation in your airways, especially the kind caused by allergic (eosinophilic) asthma.


🧪 What Does a FeNO Test Involve?

It’s quick and painless:

  • You blow slowly into a handheld machine

  • It measures the level of nitric oxide in parts per billion (ppb)

  • You get the result right away — often within a few minutes

No needles. No blood tests. Just a long, steady breath.


📉 What Does a Low FeNO Mean?

A low FeNO reading usually means that:

  • Your airways aren’t inflamed from allergy (at that moment)

  • Your asthma or ABPA may be well controlled

  • Or, your inflammation may not be the "eosinophilic" type (there are other types)

But it’s not the full picture — you can still have symptoms even if your FeNO is low. It just means the type of inflammation may be different or currently under control.


📈 What Does a High FeNO Mean?

A high FeNO result (often above 50 ppb in adults) suggests:

  • You may have active allergic inflammation in your lungs

  • Your asthma may not be well controlled

  • You may need a review of your medications, especially inhaled steroids

FeNO can also rise if you’ve been exposed to allergens (like dust or mould), or if you’ve not been taking your preventer inhaler regularly.


🌡️ What About FeNO in ABPA?

People with ABPA often have high levels of inflammation in their lungs due to allergy to Aspergillus fumigatus. This usually causes:

  • High FeNO (due to allergic response)

  • High IgE levels in the blood

  • Frequent asthma symptoms or flare-ups

BUT — FeNO may drop if you’re taking steroids, especially oral steroids, as they reduce airway inflammation. So a low FeNO doesn’t always mean your condition is inactive — it may just be well treated at the time.


🧠 Why Is FeNO Useful?

FeNO is a helpful tool for your doctor to:

  • Confirm a diagnosis of allergic asthma or ABPA

  • Check how well your treatment is working

  • Spot when inflammation is rising — even before symptoms worsen

  • Decide if you might benefit from a change in treatment (like biologics)

It’s just one piece of the puzzle — along with symptoms, blood tests (like IgE or eosinophils), CT scans, and your response to treatment.


💬 Final Thoughts

FeNO testing is a valuable, non-invasive way to check for allergic inflammation in the lungs. If you have asthma or ABPA, it can help your doctors better understand what’s going on inside your lungs — and how best to treat it.

If your FeNO is low but you still have symptoms, don’t panic — talk to your team. It just means the inflammation might be of a different kind, or affecting different parts of the lungs.

Always remember: Your symptoms matter too, not just the numbers on a machine.


Understanding IgE Levels in ABPA: What They Mean, How They Change, and What to Expect

If you’ve been diagnosed with Allergic Bronchopulmonary Aspergillosis (ABPA) or are being assessed for it, you may have heard that your IgE level is high. This can feel alarming, especially if treatment hasn’t yet been started. You might be wondering: What does a high IgE actually mean? How do treatments affect it? And what happens if treatment is stopped?

This article aims to explain what IgE levels tell us in ABPA, how they change over time, and how they’re used to guide treatment.


🧪 What is IgE and Why Is It Important in ABPA?

IgE (Immunoglobulin E) is a type of antibody made by your immune system when it overreacts to allergens. In ABPA, the immune system has an allergic-type response to the fungus Aspergillus fumigatus, which is commonly found in the environment. This immune overreaction leads to inflammation in the lungs, mucus buildup, and potential long-term lung damage.

A raised total IgE level:

  • Helps support a diagnosis of ABPA.

  • Is used by doctors to track how active the disease is.

  • Can help monitor how well treatment is working, and whether the disease is flaring up again.

While a high IgE level alone doesn’t always mean you feel worse, it often reflects that the allergic inflammation is active and needs managing.


💊 How Is IgE Reduced in ABPA?

Treatments for ABPA aim to bring down inflammation in the lungs, and when that happens, IgE levels often fall as well. There are three main types of treatment:

1. Steroids (e.g. prednisolone)

  • These are often used as the first treatment for ABPA.

  • They can bring down IgE levels within a few weeks, and help improve breathing and reduce mucus.

  • However, when steroids are stopped, IgE levels often rise again unless other treatments are also used.

2. Biologic therapies (e.g. omalizumab, mepolizumab, dupilumab)

  • These newer treatments target specific parts of the immune system that drive allergic inflammation.

  • They may help keep IgE levels lower over the long term and reduce the need for steroids.

  • In some cases, IgE may remain stable for months or years while on biologics, though responses vary from person to person.

3. Antifungal medication (e.g. itraconazole, voriconazole)

  • These drugs reduce the amount of Aspergillus in the lungs, which may reduce the allergic reaction.

  • They may help stabilise IgE levels but are usually not enough on their own for active ABPA.


⏱️ What Happens When Treatment Stops?

One of the most common concerns among patients is how long IgE stays low once treatment is stopped.

  • After stopping steroids, IgE levels often begin to rise again within a few weeks to a few months, especially if no other treatment is in place.

  • After stopping biologics, the return of symptoms and rise in IgE may happen more slowly — over several months — but varies from person to person.

  • If fungal exposure continues (e.g. in a damp or mouldy home), or the underlying immune reaction stays active, IgE is more likely to increase again.

It’s important to remember that monitoring IgE over time helps your doctor decide whether ABPA is active again and whether a change in treatment is needed.


🧠 Why Might Treatment Be Delayed?

Not everyone with a high IgE level is started on treatment right away. Your doctor may be:

  • Waiting for more information, such as CT scan results or lung function tests.

  • Being cautious about starting long-term steroids, especially if you've had side effects before.

  • Considering alternative treatment options like antifungals or biologics.

  • Monitoring to see if symptoms improve on their own or remain stable.

If you're not receiving treatment and you're unsure why, it's completely reasonable to ask for clarification — or to seek a second opinion.


👥 What Do Other Patients Say?

Many people with ABPA share similar experiences:

  • “Steroids helped quickly, but the effect didn’t last after I stopped.”

  • “I’ve been stable on a biologic and haven’t needed steroids in months.”

  • “It took a long time to get diagnosed — I had to ask lots of questions and push for answers.”

  • “My IgE rose again when I was exposed to damp or dusty environments.”

Your experience might be different, but it can be helpful to hear from others and learn what has worked for them.


Key Points to Remember

  • A raised IgE level is a common and important feature of ABPA.

  • IgE usually falls during treatment and rises again when treatment stops — especially if nothing else is done to control the inflammation.

  • Steroids work quickly, but effects often wear off without long-term planning.

  • Biologics and antifungals may help maintain lower IgE and reduce flares.

  • If you feel uncertain about your care, seeking a second opinion is perfectly appropriate.


Tip: Keep a personal record of your IgE levels, symptoms, and any treatments you're on. This can help you and your doctor spot patterns and make informed decisions together.


Understanding the Different Types of Chronic Pulmonary Aspergillosis (CPA)

CPA is a long-term lung condition caused by a common fungus called Aspergillus. It usually affects people who already have lung damage — from infections like tuberculosis (TB), conditions like COPD or asthma, or diseases such as sarcoidosis.

There are five main types of CPA. Knowing which one you have can help guide your treatment and follow-up.


🟠 1. Chronic Cavitary Pulmonary Aspergillosis (CCPA)

Most common form

  • Caused by Aspergillus growing in one or more cavities in the lungs

  • Cavities may slowly get larger or thicker

  • Often develops in people with previous lung disease

Symptoms:

  • Long-term cough

  • Fatigue and weight loss

  • Breathlessness

  • Sometimes mild or moderate coughing up blood

Treatment: Long-term antifungal tablets (e.g. itraconazole or voriconazole)


⚠️ 2. Chronic Fibrosing Pulmonary Aspergillosis (CFPA)

Advanced stage of CPA

  • Happens when long-term infection causes lung scarring (fibrosis)

  • Lungs become stiff, making breathing harder

Symptoms:

  • Worsening breathlessness

  • Low oxygen levels

  • Severe fatigue

Treatment: Focuses on antifungals, symptom relief, and oxygen if needed


🟢 3. Simple Aspergilloma

A single fungal ball in a lung cavity

  • A round ball of fungus (aspergilloma) forms in an existing lung cavity

  • Often found during scans done for other reasons

  • Some people have no symptoms at all

Main risk: Coughing up blood (sometimes serious)

Treatment:

  • Monitoring if mild

  • Surgery or embolisation if bleeding occurs


🔴 4. Subacute Invasive Aspergillosis (SAIA or CNPA)

Faster-moving form of CPA

  • Occurs over weeks to months

  • Often seen in people with weaker immune systems (e.g. due to diabetes, steroids, or alcohol dependence)

  • Infection starts to invade deeper lung tissue

Symptoms:

  • Fever

  • Worsening breathlessness

  • Severe weight loss

Treatment: Prompt antifungal treatment and close medical monitoring


🟡 5. Aspergillus Nodules

Small lumps caused by Aspergillus

  • These are solid nodules in the lungs, often found by chance on a CT scan

  • They may be mistaken for cancer at first

  • Often cause no symptoms

Treatment:

  • Usually watch and wait

  • Sometimes surgery or biopsy if uncertain


🩺 Why Knowing Your CPA Type Matters

Understanding your CPA type helps your medical team:

  • Choose the best treatment for you

  • Monitor for bleeding or lung damage

  • Decide when to repeat scans or adjust medication


💬 Questions to Ask Your Doctor

  • Which type of CPA do I have?

  • Will I need long-term antifungal treatment?

  • How often should I have scans or blood tests?

  • What should I do if I cough up blood?


🧘 Final Note

CPA is a chronic condition, but many people manage it well with the right treatment and regular check-ups. You are not alone — support and information are available.


🌿 The Different Forms of ABPA

Understanding Your Diagnosis and What It Means

Allergic Bronchopulmonary Aspergillosis (ABPA) is a condition where your immune system overreacts to a fungus called Aspergillus fumigatus, which can be found in air, soil, and compost. This allergic reaction happens mostly in people with asthma or bronchiectasis.

But not everyone with ABPA has the same experience. Doctors now recognise that ABPA can appear in several different forms or stages, depending on how far it has progressed and what’s happening in your lungs.

Here’s a simple guide to help you understand where you might fit — and what it means for your care.


✅ 1. ABPA-S (Serologic ABPA) — The early stage

This is the mildest form of ABPA. It means your immune system is reacting to Aspergillus, but your lungs haven’t been damaged yet.

What’s usually found:

  • High levels of IgE (allergy antibodies)

  • Positive test for Aspergillus-specific IgE

  • Normal or near-normal scans (X-ray or CT)

  • Asthma or mild chest symptoms

🟢 This form is often picked up with blood tests before any permanent changes in the lungs happen.


🟠 2. ABPA-CB — ABPA with Central Bronchiectasis

This is a more typical form of ABPA, where the ongoing allergic reaction has started to damage your airways. “Bronchiectasis” means some airways have become widened and scarred.

What’s usually found:

  • All of the features above plus

  • Changes on a CT scan showing central bronchiectasis

  • More mucus, coughing, or breathlessness

🟠 This form may need regular treatment to reduce inflammation and protect the lungs.


🔴 3. Severe ABPA — ABPA with frequent flares

This isn’t a separate type, but a more active or harder-to-control version of ABPA.

What’s usually happening:

  • Frequent flare-ups (exacerbations)

  • Need for ongoing steroids or antifungals

  • Possible use of biologic medicines (e.g. Xolair/omalizumab)

  • More serious asthma symptoms

🔴 This form can still be well-managed, but needs close monitoring and a good treatment plan.


⚠️ 4. ABPA-CPF — ABPA with Lung Scarring (Fibrosis)

This is the late stage of ABPA, where ongoing inflammation over many years has caused permanent damage to the lungs. It’s now much rarer thanks to earlier diagnosis and treatment.

What’s usually found:

  • Extensive scarring or fibrosis on lung scans

  • Breathlessness or tiredness

  • May overlap with another condition called chronic pulmonary aspergillosis (CPA)

⚠️ This stage needs careful support, but many people can still manage symptoms and improve quality of life.


📈 How doctors track your ABPA

Some doctors will also use stages to describe how your ABPA is behaving, though this does not comply with the most recent guidelines (ISHAM 2024):

  • Stage 0 – No symptoms, but abnormal blood test

  • Stage 1 – Newly diagnosed (active symptoms)

  • Stage 2 – Responding to treatment

  • Stage 3 – In remission (no active disease)

  • Stage 4 – Flare-up

  • Stage 5 – Long-term lung damage (fibrosis)


🩺 Why this matters to you

Knowing what form of ABPA you have helps you and your healthcare team:

  • Choose the right treatments

  • Decide how often you need scans or blood tests

  • Spot early signs of flare-ups

  • Protect your lungs from long-term damage


💬 Final message:

No matter which form you have, there are treatments that work. Many people with ABPA live full lives with the right support.
If you're unsure what form of ABPA you have, ask your doctor — it can help you understand what to expect and how to take care of your lungs.


Allergic Bronchopulmonary Aspergillosis (ABPA) Without Asthma: A Hidden Reality

Most people – including many doctors – associate Allergic Bronchopulmonary Aspergillosis (ABPA) almost exclusively with asthma or cystic fibrosis. In fact, the current diagnostic criteria for ABPA often assume the presence of asthma as a prerequisite. But what happens when a patient has all the features of ABPA… without ever having had asthma?

This article explores the possibility – and growing recognition – of ABPA without asthma.


🔍 What Is ABPA?

ABPA is an allergic (hypersensitivity) reaction to the fungus Aspergillus fumigatus, which can colonise the lungs and cause:

  • Severe allergic inflammation

  • Damage to lung tissue (bronchiectasis)

  • High levels of IgE (often >1000 IU/mL)

  • Positive skin tests or blood tests for Aspergillus

Traditionally, ABPA is diagnosed in people with asthma or cystic fibrosis, where the airways are already vulnerable.


❗But Can ABPA Occur Without Asthma?

Yes. Though uncommon, there are confirmed cases where ABPA occurs in people who:

  • Do not have asthma

  • Have no wheeze, breathlessness or variability in symptoms

  • Show no reversibility on a bronchodilator test

  • May not respond to inhaled corticosteroids

This presentation is now increasingly recognised – particularly:

  • After viral infections like COVID-19

  • In people exposed to environmental moulds

  • In those with no personal or family history of asthma


🧪 Diagnostic Clues

Patients with ABPA but no asthma typically still show:

  • Very high total IgE levels

  • Positive Aspergillus-specific IgE and IgG

  • Radiological changes like central bronchiectasis

  • Sometimes eosinophilia in blood

But they do not show:

  • Classic asthma symptoms (e.g. wheeze, reversible breathlessness)

  • Improvement with bronchodilators

  • Variable peak flow readings


🧬 How Might This Happen?

There are a few theories:

  • Some people have a strong allergic immune response (IgE-driven) to Aspergillus alone, even without underlying asthma

  • COVID-19 and other infections may prime the immune system or damage airways enough to allow fungal colonisation

  • Not all bronchial hypersensitivity is asthma — the airway inflammation in ABPA is unique and not always “asthmatic” in pattern


✅ What Tests Can Help Confirm or Rule Out Asthma?

For patients who have ABPA but no clear asthma symptoms:

  • Bronchodilator reversibility test → May be negative

  • Methacholine or histamine challenge test → Gold standard for confirming asthma

  • FeNO test → Measures eosinophilic airway inflammation (may be high in both ABPA and asthma)

  • Peak flow monitoring → Often stable in ABPA without asthma

These tests can help clarify the diagnosis and prevent mislabeling patients as asthmatic when they are not.


🧭 Why Does It Matter?

Correct diagnosis matters because:

  • Not all ABPA patients benefit from inhaled corticosteroids or asthma drugs

  • Treatment should be tailored — e.g. antifungals and oral steroids for ABPA, but not unnecessary asthma medications

  • Misdiagnosis may delay the right treatment and overburden patients


🩺 A Call to Clinicians

If a patient has high IgE, bronchiectasis, and strong Aspergillus sensitisation — but no clinical asthma — consider ABPA without asthma.

Request confirmatory tests before labeling someone asthmatic for life. In these rare cases, asthma criteria do not fully apply — but the patient still needs support for ABPA.


🧾 Summary

Feature ABPA With Asthma ABPA Without Asthma
Wheeze/breathlessness Common May be absent
Bronchodilator response Often positive Usually negative
Total IgE High High
Aspergillus IgE/IgG Positive Positive
Imaging (HRCT) Bronchiectasis Bronchiectasis

🙋 What Can Patients Do?

If you’ve been diagnosed with ABPA but don’t believe you have asthma:

  • Ask your doctor about further testing to confirm or rule out asthma

  • Keep a record of your symptoms, peak flow (if used), and medication response

  • Discuss your IgE levels, CT scan results, and whether other diagnoses (e.g. chronic pulmonary aspergillosis) might apply


If Aspergillus-specific IgE is already positive, why bother testing IgG too?

🧠 ABPA: A quick reminder

ABPA (Allergic Bronchopulmonary Aspergillosis) is an allergic reaction to the fungus Aspergillus fumigatus, most commonly in people with asthma or cystic fibrosis.

Your immune system reacts in two key ways:

  1. IgE antibodies – part of an allergic response (like in hay fever or asthma).

  2. IgG antibodies – part of a chronic or repeated exposure response, often related to inflammation or tissue damage.


💡 Your main question:

If ABPA-specific IgE is already positive, why bother testing IgG too? Shouldn’t it also be positive?

Not always. Here’s why both are useful and not redundant:


🔬 Why test IgG if IgE is already positive?

✅ 1. They tell us different things:

  • IgE (specific to Aspergillus) → Shows allergic sensitisation. This is key for diagnosis.

  • IgG (specific to Aspergillus) → Suggests immune system has been exposed repeatedly or persistently to Aspergillus, usually through colonisation in the lungs.

You can have:

  • High IgE but normal IgG — early or milder ABPA.

  • High IgE and high IgG — more established disease, or significant fungal colonisation.

  • High IgG but normal IgE — maybe chronic pulmonary aspergillosis (CPA), not ABPA.

✅ 2. It helps to rule out other conditions

For example:

  • CPA is often IgG positive but IgE normal.

  • ABPA is usually IgE high, often with IgG also raised, but not always.

So, IgG helps confirm, clarify, or differentiate between Aspergillus-related conditions.

✅ 3. It adds confidence to the diagnosis

If both Aspergillus-specific IgE and IgG are raised, it makes the diagnosis of ABPA stronger — especially when imaging shows mucus plugging, bronchiectasis, or infiltrates.


🧪 Summary:

Test What it tells us Role in ABPA
Aspergillus-specific IgE Allergic sensitisation Core to diagnosis
Aspergillus-specific IgG Immune exposure/colonisation Supports diagnosis & helps rule out other forms

🧍🏻 Simple analogy:

Think of:

  • IgE like the smoke alarm — it reacts to allergens quickly.

  • IgG like the carbon monoxide detector — it reacts to long-term exposure that might not cause an immediate “allergic” fire but still shows something’s wrong.


🩸 Understanding Blood Tests for Aspergillosis: A Patient Guide

If you’ve been told you have ABPA, CPA, or another form of aspergillosis, your doctors may run several blood tests. These tests help confirm the diagnosis, guide treatment, and monitor your progress.

Please remember that blood tests only form part of the process of diagnosing and managing aspergillosis - scans, case history, symptoms and more are also essential parts of a doctor's reasoning. To get a complete picture of your diagnosis, we need all of the parts.

Here’s a breakdown of what each test is, why it’s done, and what it means:


1. Total IgE (Immunoglobulin E)

🧪 What it is: A measure of all the allergy-related antibodies in your blood.
📌 Why it's used:

  • In ABPA, total IgE is usually very high — often above 1,000 IU/mL.

  • Doctors use it to help diagnose ABPA and then to monitor flare-ups or improvements.

💡 What it tells you:

  • High IgE suggests an allergic response, often to Aspergillus.

  • A fall in IgE after treatment often shows you're getting better.

  • A sudden rise might mean a flare-up.


2. Aspergillus-specific IgE

🧪 What it is: A test that looks for allergy antibodies targeting Aspergillus fumigatus.
📌 Why it's used:

  • Helps confirm whether your immune system is reacting to Aspergillus.

  • It’s part of the diagnosis for ABPA and SAFS (Severe Asthma with Fungal Sensitisation).

💡 What it tells you:

  • A positive result means you are sensitised (allergic) to Aspergillus.

  • It doesn’t prove infection — just allergy.


3. Aspergillus-specific IgG

🧪 What it is: A test for long-term antibody response to Aspergillus.
📌 Why it's used:

  • Important in diagnosing Chronic Pulmonary Aspergillosis (CPA).

  • Also used in Aspergillus bronchitis.

💡 What it tells you:

  • High IgG means your immune system has been exposed to Aspergillus over time, likely indicating long-term infection.

  • It’s not an allergy test — it looks for signs of chronic infection or colonisation.


4. Aspergillus precipitins (Immunodiffusion or counter-immunoelectrophoresis)

🧪 What it is: An older test to detect antibodies to Aspergillus proteins.
📌 Why it's used:

  • Sometimes used in CPA or fungal ball (aspergilloma) diagnosis.

  • Less sensitive than IgG ELISA but still used in some labs.

💡 What it tells you:

  • A positive test supports the diagnosis of chronic infection.


5. Eosinophil Count

🧪 What it is: A blood count of a type of white cell linked to allergy and inflammation.
📌 Why it's used:

  • In ABPA, eosinophils are often elevated, especially during flares.

  • It helps show how much inflammation is present.

💡 What it tells you:

  • High eosinophils support a diagnosis of allergic inflammation.


6. Galactomannan (in blood or BAL fluid)

🧪 What it is: A test for fungal cell wall fragments released by Aspergillus, useful when detecting the patient's immune response to infection is limited.
📌 Why it's used:

  • Mainly used in hospitals to detect invasive aspergillosis, especially in people with weakened immune systems.

💡 What it tells you:

  • A positive result may suggest active infection — but false positives can occur.


7. Beta-D-Glucan (BDG)

🧪 What it is: A general marker of fungal infection in the bloodstream.
📌 Why it's used:

  • Used to detect invasive fungal infections, especially in ICU patients.

💡 What it tells you:

  • Not specific to Aspergillus, but may support the diagnosis of serious fungal disease.


🧭 Putting It All Together

Different types of aspergillosis need different combinations of tests:

Condition Useful Tests
ABPA Total IgE, Aspergillus-specific IgE, eosinophils
SAFS Aspergillus-specific IgE only
CPA Aspergillus-specific IgG, precipitins, imaging
Aspergillus bronchitis Aspergillus IgG, culture, sometimes IgE
Invasive Aspergillosis Galactomannan, Beta-D-Glucan, CT scan, biopsy (in hospital settings)

🗨️ Questions to Ask Your Doctor

  • What type of aspergillosis do I have?

  • Which tests are being used to monitor my condition?

  • Should I expect these results to go up and down?

  • What symptoms should I report if things change?


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.


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