**Where Do All These Immune Cells Live, and Where Are They Made?

A Simple Guide for Patients and Carers**

When we talk about T cells, B cells, eosinophils, mast cells, IgE, IgG, and other immune system parts, it’s natural to wonder:

Where are these cells actually made?
Where do they live in the body?
Where do they go when you’re ill?

Here is a simple explanation.


🧱 1. Most immune cells are MADE in the bone marrow

Bone marrow is the soft tissue inside your bones (especially the pelvis, spine, ribs, skull, and sternum).

Inside this marrow are stem cells, which are the “mother cells” that can turn into:

  • red blood cells

  • white blood cells

  • platelets

Almost all immune cells begin their life in the bone marrow, including:

  • B cells

  • eosinophils

  • mast cell precursors

  • neutrophils

  • monocytes

  • basophils

The bone marrow is like the main factory for your entire immune system.


🫀 2. T cells are trained in the thymus

After T cells are created in the bone marrow, they travel to the thymus — a small organ behind the breastbone.

The thymus is like a school where T cells learn:

  • what is safe

  • what is dangerous

  • how to avoid attacking the body itself

This training is essential for preventing autoimmune diseases.

After training, T cells spread through the body.


🩸 3. Immune cells travel in the blood and lymph

Once made, immune cells circulate around the body like security guards on patrol.

They travel through:

Blood

This carries cells quickly to any part of the body.

Lymph system

A drainage and communication network that runs alongside the bloodstream.

Lymph nodes (in the neck, armpits, groin) act like checkpoints, where:

  • immune cells meet

  • information is exchanged

  • inflammation signals get amplified

If your glands are swollen during illness, that’s because immune cells are gathering there.


🫁 4. Many immune cells live in tissues, not just in the blood

Some immune cells settle in certain places:

Mast cells

Live in tissues such as:

  • lungs

  • sinuses

  • skin

  • gut

  • blood vessels

They wait there like "alarm sensors," ready to react if something enters the tissue.

Macrophages

Live in tissues and “eat” germs.

Eosinophils

Move into tissues during allergy or asthma flare-ups.

T cells and B cells

Live in:

  • lymph nodes

  • spleen

  • tonsils

  • tissues throughout the body

  • airway lining in people with asthma or ABPA


🧫 5. Where antibodies (IgE, IgG) come from

Antibodies are made by plasma cells, which are specialised B cells.

These plasma cells usually live in:

  • the bone marrow

  • lymph nodes

  • spleen

  • airway tissues (especially in chronic inflammation)

So:

  • IgE is mostly made in tissues involved in allergy (lungs, sinuses, skin).

  • IgG is made in bone marrow and lymph tissues to provide long-term protection.

Antibodies then circulate in the blood, ready to recognise anything they have been trained to detect.


🧬 Where these cells actually are, in simple terms:

Immune Cell / Antibody Where It Is Made Where It Lives / Works
B cells Bone marrow Lymph nodes, blood, tissues
Plasma cells (make antibodies) Bone marrow / lymph nodes Bone marrow, tissues
T cells Bone marrow → trained in thymus Blood, lymph nodes, organs
IgE antibodies Plasma cells in tissues Lungs, skin, blood
IgG antibodies Plasma cells Blood (body-wide protection)
Eosinophils Bone marrow Blood → lungs during flare-ups
Mast cells Bone marrow (as precursors) Lungs, skin, sinuses, gut
Neutrophils Bone marrow Blood → infection sites

🧠 6. How this applies to aspergillosis

In ABPA

  • IgE is made in the lung tissues.

  • Mast cells in the lungs release histamine.

  • Eosinophils move from the bone marrow into the airways.

In CPA

  • IgG is made in bone marrow in response to chronic infection.

  • T cells gather in lung cavities and damaged tissue.

In fungal asthma / SAFS

  • Mast cells and eosinophils in the lungs respond strongly to triggers.

Understanding where these cells come from and where they live helps explain why:

  • symptoms can flare suddenly

  • blood test levels change

  • treatments like steroids or biologics work

  • inflammation can persist even when scans look stable


🏁 Simple takeaway

  • Your bone marrow makes most of your immune cells.

  • Your thymus trains T cells.

  • Immune cells patrol your blood and lymph system.

  • Many immune cells live long-term in your lungs, skin, and tissues.

  • Antibodies are made by plasma cells in bone marrow and lymph nodes.

  • In aspergillosis, the lungs become a major “immune battlefield.”

Next articles:


**Eosinophils and Type-2 Inflammation:

What Aspergillosis Patients Need to Know**

Part of the Aspergillosis Immune System Knowledge Hub


Eosinophils are a type of white blood cell central to allergy, asthma, and ABPA. They play a major role in symptoms, flare-ups, mucus plugging, and treatment responses.

This article explains eosinophils in simple terms.


🧬 1. What Are Eosinophils?

Eosinophils are immune cells filled with granules containing powerful enzymes.
They normally help:

  • fight parasites

  • regulate allergic inflammation

  • repair tissues

  • produce important immune signals

But in excess, they can cause damage — especially in the lungs.


🔥 2. Eosinophils in the Lungs

Activated eosinophils release their granules into airway tissues, causing:

  • swelling

  • increased mucus

  • airway narrowing

  • cough sensitivity

  • wheezing

  • breathlessness

This makes them key players in allergic and fungal-related lung disease.


🌟 3. Eosinophils in ABPA

Eosinophils are highly active in ABPA.

ABPA involves a strong “type-2” allergic response to Aspergillus, including:

  • high IgE

  • mast cell activation

  • large numbers of eosinophils

  • thick, sticky mucus

  • airway obstruction

  • repeated flare-ups

Eosinophils contribute significantly to long-term lung damage if not controlled.


🌬 4. Eosinophils in Severe Asthma and SAFS

In severe or allergic asthma:

  • eosinophils can be persistently high

  • they drive airway swelling

  • they increase sensitivity to triggers

  • they worsen recovery after infection

In SAFS, eosinophils may be moderately raised but symptoms can still be severe.


🦠 5. Eosinophils in CPA

In CPA, eosinophils are not usually the dominant cell, but they still matter when patients also have:

  • asthma

  • ABPA overlap

  • fungal allergy

  • airway hypersensitivity

  • steroid withdrawal flare-ups


🔗 6. How Eosinophils Link to Other Immune Cells

They interact with:

  • IgE → recruits eosinophils

  • T-helper cells (Th2) → tell bone marrow to make more

  • Mast cells → release histamine that pulls eosinophils into tissues

  • Airway lining cells → release distress signals

This is why severe allergic pathways often involve all three:
IgE → mast cells → eosinophils


💊 7. Treatments That Target Eosinophils

✔ Steroids (oral or inhaled)

Suppress eosinophil activity.

✔ Biologics

Directly reduce eosinophils:

  • Mepolizumab (anti-IL-5)

  • Benralizumab (anti-IL-5 receptor)

  • Reslizumab (anti-IL-5 infusion)

Reduce eosinophil recruitment:

  • Dupilumab (anti-IL-4/IL-13)

  • Tezepelumab (broad upstream suppression)

These can transform life for patients with severe asthma or ABPA.


🧠 8. Summary

Eosinophils are key drivers of:

  • flare-ups

  • mucus plugging

  • wheeze

  • breathlessness

  • airway damage

Understanding them helps patients:

  • interpret blood tests

  • understand biologic treatments

  • recognise flare-up patterns

  • manage ABPA and asthma more confidently

Next articles:


**What Happens in Autoimmune Disease?

(Explained with Addison’s Disease)**

Part of the Aspergillosis Immune System Knowledge Hub


Autoimmune disease occurs when the immune system mistakenly attacks the body’s own tissues. This is different from allergy, infection, or inflammation caused by fungal disease. Addison’s disease is a clear example of autoimmunity and helps explain how this process works.


1. Autoimmunity = Loss of Immune Tolerance

In autoimmune disease:

  • the immune system starts recognising the body’s own tissues as “foreign”

  • T cells and B cells become misdirected

  • autoantibodies form

  • inflammation destroys healthy cells

This process develops over months or years.


🧬 2. What Specifically Happens in Addison’s Disease?

Addison’s disease is caused by an autoimmune attack on the adrenal cortex, the part of the adrenal gland that makes:

  • cortisol

  • aldosterone

  • DHEA (adrenal androgens)

The steps include:

1. Loss of tolerance
The immune system mistakenly targets adrenal enzymes (especially 21-hydroxylase).

2. Autoantibodies form
These can be detected in blood tests.

3. Cytotoxic T cells attack adrenal tissue
Gradually destroying hormone-producing cells.

4. Hormone levels fall
Leading to:

  • severe fatigue

  • weight loss

  • low blood pressure

  • salt loss

  • nausea

  • risk of adrenal crisis

Addison’s must be treated with lifelong hormone replacement.


🔄 3. Why Does Autoimmunity Happen?

Factors include:

✔ Genetic susceptibility (HLA types)

✔ Prior viral infection or severe inflammation

✔ Stressful life events

✔ Regulatory T-cell failure

✔ Microbiome disruption

✔ Hormonal influences

Importantly:
Autoimmune disease is never the patient’s fault.


🆚 4. How Autoimmunity Differs from Aspergillosis

Aspergillosis Autoimmune Disease
Driven by external organism (Aspergillus fungus) Driven by immune system attacking “self”
ABPA → IgE allergies; CPA → IgG infection response Autoantibodies + T-cell attack
Treatment aims at fungus + inflammation Treatment replaces missing hormones
Damage = collateral Damage = direct

Some patients live with both conditions (e.g., ABPA + adrenal insufficiency), but they arise via very different mechanisms.


🧠 5. Key Message

Autoimmune disease results from a failure of immune tolerance, not from weakness, lifestyle, or exposure. Understanding this helps patients feel more in control and reduces self-blame.


Next articles:


**How the Immune System Knows What Is “Self”:

A Patient-Friendly Explanation**

Part of the Aspergillosis Immune System Knowledge Hub


Your immune system must be aggressive enough to fight infection — yet gentle enough not to damage your own organs. To achieve this balance, it uses several sophisticated systems to distinguish “self” from “non-self.”


🆔 1. Identity Badges on Every Cell (MHC)

All your cells display special proteins called MHC molecules, which act like ID badges.

They say:
“I belong to this body — do not attack me.”

Immune cells constantly check these badges.

  • Normal MHC → safe

  • Missing/damaged MHC → suspicious

  • Viral or fungal proteins presented on MHC → attack triggered


🧪 2. Immune Training in the Thymus

T cells undergo training in the thymus, where:

  • harmful T cells that attack your own tissues are destroyed

  • safe T cells are allowed to mature

  • tolerance is established early in life

This is called central tolerance.


🛡 3. Regulatory T Cells — the Immune “Brakes”

These cells prevent overreaction and calm inflammation.
They stop the immune system attacking:

  • your lungs

  • your adrenal glands

  • your skin

  • your nerves

  • any part of your own body

If regulatory T cells fail, autoimmune disease can develop.


🚨 4. Danger Signals — The Immune System Reacts to Threats, Not Just Foreign Material

The immune system does not attack everything foreign.
It attacks things that appear:

  • dangerous

  • infected

  • damaged

  • inflamed

This is why harmless substances (pollens, dust, Aspergillus spores) can become allergens — the immune system labels them incorrectly.


🦠 5. The Microbiome Helps Train Immune Tolerance

Healthy bacteria in the gut, skin, and lungs help the immune system learn:

  • what to attack

  • what to ignore

  • how strongly to react

A disrupted microbiome can increase the risk of allergy and autoimmunity.


🧠 6. Why This Matters for Aspergillosis Patients

Understanding immune tolerance helps explain:

  • why some people get allergy (ABPA)

  • why some people get chronic infection (CPA)

  • why a few people develop autoimmune issues, including Addison’s or thyroid disease

  • how treatments such as biologics work

  • why inflammation can flare even without new infection


Next articles:


**Pain Perception and Aspergillosis:

Why It Matters — and What Help Is Available**

Living with aspergillosis—whether Chronic Pulmonary Aspergillosis (CPA), Allergic Bronchopulmonary Aspergillosis (ABPA), Aspergillus bronchitis, or Severe Asthma with Fungal Sensitivity (SAFS)—can mean coping with symptoms that change day to day.
Pain, breathlessness, muscle aches, fatigue and joint discomfort are common. What many people don’t realise is that how the body perceives and processes pain plays a major role in how these symptoms feel — and how well they can be managed.

Understanding pain perception doesn’t mean your symptoms aren’t real. It means understanding why pain behaves the way it does in chronic illness — and how to gain more control.


1. Why pain perception matters in aspergillosis

Pain is produced by the nervous system, and is influenced by:

  • Inflammation in the lungs or sinuses

  • Muscle strain from coughing or altered breathing

  • Reduced fitness after flare-ups

  • Long-term corticosteroid use

  • Adrenal insufficiency

  • Stress, uncertainty, poor sleep, and emotional load

Pain is therefore a mix of bodily changes and how the brain interprets signals.
Both are real. Both deserve attention.


2. Muscle changes and increased sensitivity

People with aspergillosis may experience:

  • Weakened rib, back, and shoulder muscles

  • Reduced leg strength

  • Joint instability

  • Muscle fatigue leading to higher pain sensitivity

Everyday movements can feel more painful, and pain can worsen breathlessness. Many people fall into a cycle: flare-up → rest → muscle weakening → more pain → more breathlessness → more rest.

Understanding this cycle helps break it.


3. Stress, sleep and emotions influence pain

Pain becomes stronger when:

  • You are tired

  • You feel anxious, unsafe, or overwhelmed

  • Your symptoms are unpredictable

  • You have recently been in hospital

  • You are caring for someone who is unwell

This does not mean pain is psychological.
It means the nervous system becomes more alert, so signals feel louder.

Carers experience this too.


4. Why understanding pain helps you manage symptoms

Learning about pain perception helps you:

  • Pace activity wisely

  • Avoid panic when symptoms spike

  • Identify muscular vs inflammatory discomfort

  • Communicate clearly with clinicians

  • Reduce stress-driven symptom amplification

  • Prevent flare-ups by calming the nervous system

It’s not about ignoring symptoms — it’s about understanding them so you can respond safely and confidently.


5. NHS resources that can help

Below are useful links recommended across NHS pain services.


🔹 NHS self-help guidance on long-term pain

These pages offer practical advice on managing persistent pain, pacing, movement, and everyday strategies:

How to get NHS help for your pain
https://www.nhs.uk/live-well/pain/how-to-get-nhs-help-for-your-pain/

10 ways to reduce pain
https://www.nhs.uk/live-well/pain/10-ways-to-ease-pain/

These guides are suitable for people with chest pain, muscular pain, fatigue and inflammation linked to lung disease.


🔹 NHS Pain Management Programmes (PMP)

Many NHS Trusts run Pain Management Programmes. These provide a combination of physiotherapy, psychology, pacing education, flare-up planning, and medication review.

Examples of NHS PMP resources:

Royal Orthopaedic Hospital – PMP information
https://roh.nhs.uk/services-information/pain-management/pain-management-programme

Ashford & St Peter’s Hospitals – Pain Management Programme
https://www.ashfordstpeters.nhs.uk/the-pain-management-programme

Gloucestershire Hospitals – Pain Management Options
https://www.gloshospitals.nhs.uk/our-services/services-we-offer/pain-management-service/management-options-pain/

Speak to your GP or specialist team if you want a referral.


🔹 The Pain Toolkit (NHS-endorsed self-management booklet)

Widely used by NHS pain services and physiotherapy teams.

PDF:
https://www.nhsfife.org/media/c349s6xo/nhs-fife-pain-toolkit.pdf

This guide covers pacing, flare-up planning, problem-solving, emotional wellbeing and shared decision-making.


🔹 NHS Talking Therapies (for stress-related pain amplification)

If stress, anxiety or sleep disturbance are worsening your pain, NHS Talking Therapies services can help.

Find your local service here:
https://www.nhs.uk/service-search/mental-health/find-a-psychological-therapies-service/

These services support people with long-term physical conditions as well as mood and anxiety problems.


🔹 Physiotherapy & pulmonary rehabilitation

These services help with:

  • Breathing pattern retraining

  • Strengthening ribs, shoulders, back, hips, and knees

  • Improving stamina and reducing breathlessness

  • Reducing muscle pain and improving posture

Ask your GP, respiratory consultant, or specialist nurse for a referral.


6. What patients and carers can start today

✔ Notice pain patterns

Track fatigue, sleep, activity, stress, and symptoms.

✔ Practice pacing

Spread tasks through the day. Avoid pushing hard on “good days” — it often leads to flare-ups.

✔ Gentle strengthening

Even small daily exercises protect joints, support breathing and lower pain sensitivity.

✔ Reduce nervous-system overload

Breathing exercises, grounding, relaxation and mindfulness calm the system that amplifies pain.

✔ Seek help early

If pain changes or worries you, involve your GP or specialist team.

✔ Carers: protect your wellbeing

Carers benefit from pacing, strengthening and psychological support just as much as patients.


7. When to seek medical review

Contact your GP or specialist team urgently if you experience:

  • Sudden new chest pain

  • Pain with fever or coughing up blood

  • Pain that stops you breathing normally

  • Severe muscle weakness

  • Persistent flare-ups despite treatment

  • Symptoms suggesting adrenal problems

Pain in aspergillosis is real, but also manageable. With the right understanding and NHS-supported tools, you can reduce flare-ups, regain confidence, and improve daily life.


⭐ Severe Asthma with Fungal Sensitisation (SAFS): The Hidden Burden Behind Difficult Asthma

Estimated prevalence: 15–30% of severe asthma patients show fungal sensitisation.

Severe Asthma with Fungal Sensitisation (SAFS) describes a group of patients with severe asthma who show sensitisation (allergy) to Aspergillus or other environmental moulds but do not meet criteria for ABPA. These patients often experience persistent inflammation, breathlessness, mucus production, and exacerbations that are not adequately controlled by standard asthma therapies.

Although SAFS is common in severe asthma clinics, it remains poorly recognised, frequently mislabelled, and rarely discussed in routine practice. Yet identifying SAFS is crucial because it opens the door to specific interventions — including antifungals or targeted biologics — that can improve symptoms and reduce hospital admissions.


How Common Is SAFS?

SAFS is more common than ABPA and CPA combined in asthma services.

Population Estimated prevalence
Moderate asthma ~5%
Severe asthma 15–30%
Patients with frequent exacerbations up to 40%
ABPA-negative patients with mucus plugging high likelihood

Across the UK, this represents tens of thousands of people.


Why SAFS Is Missed

1. The diagnosis is not widely understood

Unlike ABPA or CPA, SAFS lacks:

  • universally agreed diagnostic criteria

  • clear imaging features

  • a single confirmatory test

This leads to variability in thinking and detection.


2. Symptoms mimic uncontrolled asthma

SAFS patients typically experience:

  • severe breathlessness

  • wheeze

  • mucus production

  • airway plugging

  • poor response to inhalers

  • frequent steroid courses

These appear indistinguishable from “difficult” or “type 2–high” asthma.


3. IgE and eosinophils may be normal

Unlike ABPA:

  • total IgE may be modest

  • Aspergillus IgE may be borderline

  • eosinophils may fluctuate, especially with steroids or biologics

Clinicians are often looking for very high IgE levels — but SAFS patients usually don’t show them.


4. Sputum and CT scans appear non-specific

Typical imaging:

  • mucus plugging

  • small-airway thickening

  • variable, patchy inflammation

  • bronchiectasis may or may not be present

Radiologists often report these changes as:

  • “consistent with asthma”

  • “post-infective”

  • “non-specific inflammatory pattern”


5. The fungal link is overlooked

Many clinicians are unfamiliar with:

  • the role of mould exposure

  • sensitisation thresholds

  • the overlap between environmental allergy and airway disease

  • when antifungals are appropriate

This leads to delays in recognising fungal-driven asthma.


Who Is at Highest Risk?

1. Severe asthma patients unresponsive to maximal inhaled treatment

Particularly those with:

  • frequent exacerbations

  • nocturnal symptoms

  • long-term steroid use

  • persistently low lung function

  • mucus plugging events


2. Patients sensitised to Aspergillus or multiple moulds

Positive skin tests or specific IgE indicate airway allergy that can drive symptoms.


3. Patients with damp or mould exposure at home or work

An important environmental factor often overlooked.


4. ABPA-negative asthma patients with mucus plugging

A large proportion of these patients fit the SAFS profile.


5. Those with co-existing bronchiectasis

Bronchiectasis amplifies the inflammatory response to fungal exposure.


Specialties That Need Greater Awareness

  • Severe asthma services & biologics clinics
    (primary diagnostic opportunity)

  • General respiratory clinics

  • Primary care & urgent care
    (patients seen frequently with “persistent asthma symptoms”)

  • Radiology
    (important for identifying mucus plugging)

  • Allergy/Immunology
    (mould sensitisation is central to diagnosis)

  • Environmental health teams
    (exposure to mould and dampness often perpetuates symptoms)

The National Aspergillosis Centre can provide specialist input when diagnosis is unclear or response to treatment is suboptimal.


Red Flags Suggesting SAFS

1. Severe asthma poorly controlled despite maximal inhalers

Including biologics (omalizumab, mepolizumab, benralizumab, dupilumab, tezepelumab).

2. Sensitisation to Aspergillus fumigatus or multiple moulds

3. Repeated mucus plugging episodes

(or “sticky mucus” symptoms)

4. More than 2–3 steroid-treated exacerbations per year

5. Asthma + bronchiectasis

Even mild bronchiectasis increases fungal risk.

6. Symptoms triggered by damp/mould exposure

7. Persistent airway inflammation despite correct inhaler technique


Misdiagnoses That Delay Recognition

  • “Difficult asthma”

  • “Brittle asthma”

  • “Post-viral inflammation”

  • “Poor adherence to inhalers”

  • “Asthma–COPD overlap”

  • “Psychogenic dyspnoea”

  • “Recurrent chest infections”

SAFS is a diagnosis hiding in these labels.


The Cost of Missed SAFS Diagnosis

For patients:

  • persistent symptoms

  • steroid dependence

  • increased risk of ABPA

  • progressive airway damage

  • hospital admissions

  • poor quality of life

  • possible career and lifestyle impact

For healthcare systems:

  • repeated A&E visits

  • asthma admissions

  • high biologic usage without adequate response

  • unnecessary antibiotics

  • escalating steroid toxicity

  • missed environmental interventions


Conclusion

SAFS is one of the most common — yet least recognised — fungal-related lung conditions. Although it lacks the dramatic imaging changes of ABPA or CPA, its impact on patients is profound.

Recognising mould sensitisation in severe asthma, understanding the role of fungal allergens, and considering targeted therapies can transform disease control. For complex cases or when the diagnosis is uncertain, referral to the National Aspergillosis Centre is recommended.

Early identification and appropriate treatment reduce steroid use, exacerbations, and long-term airway damage.


⭐ 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.


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

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

  • Thinner hips and legs

  • More weight around the waist or tummy

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


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

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

  • Breathlessness

  • Fatigue

  • Repeated chest infections

  • Less ability to walk long distances or climb stairs

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

  • Slimmer thighs

  • Smaller hips

  • Feeling weaker when getting out of a chair

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


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

Many aspergillosis patients have had:

  • Several courses of prednisolone over the years

  • High-dose inhaled steroids

  • Hydrocortisone replacement for adrenal problems

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

  • Fat and muscle reduce in the arms, hips and legs

  • More fat settles around the stomach area

  • The centre of the body becomes rounder even if the overall weight hasn’t changed much

This effect can continue long after stopping steroids.


3. Ageing naturally shifts fat towards the waist

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

  • Less around the hips and thighs

  • More around the waist

  • More “internal” fat around organs (visceral fat)

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


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

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

That’s because:

  • Muscle in the legs may be lost

  • Fat around the waist may increase

  • The total body weight doesn’t always change much

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


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

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

  • Eat less

  • Feel exhausted

  • Lose muscle faster

  • Keep or gain tummy fat

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


Is this dangerous?

Not usually on its own — but it does mean:

  • Legs may feel weaker

  • Balance and stamina can reduce

  • It may be harder to stay active

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

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


In summary

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

  • Reduced activity due to breathlessness

  • Loss of leg and hip muscle

  • Steroid effects on fat distribution

  • Natural age-related changes

  • Appetite changes during illness

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