Muscle Cramps in Aspergillosis (Including ABPA and CPA): Causes, Triggers, and What May Help

Last reviewed: March 2026
Audience: Patients, carers, and non-specialist healthcare professionals

Key Points

Muscle cramps—especially at night—are commonly reported by people with long-term lung conditions such as allergic bronchopulmonary aspergillosis (ABPA) and chronic pulmonary aspergillosis (CPA).
There is usually no single cause; cramps often result from a combination of factors including medications, fatigue, hydration, and electrolyte balance.
In CPA, additional factors such as antifungal therapy and kidney function may play an important role.
Persistent or worsening cramps should be discussed with a healthcare professional, as some causes are treatable.

Overview
Why do muscle cramps happen?
How is this linked to aspergillosis and its treatment?
Additional considerations in chronic pulmonary aspergillosis (CPA)
Common contributing factors
What may help reduce cramps
When to seek medical advice
Common questions
References

Overview

Muscle cramps are sudden, involuntary contractions of a muscle that can last from seconds to several minutes. Many people describe them as painful tightening or “locking” of the muscle, often affecting the calves, thighs, feet, or hands.

For people living with aspergillosis, including allergic bronchopulmonary aspergillosis (ABPA) and chronic pulmonary aspergillosis (CPA), cramps are frequently discussed in patient communities. They are particularly common at night and may affect sleep and quality of life.

Importantly, while cramps can be uncomfortable and sometimes severe, they are often manageable once contributing factors are identified.

Why do muscle cramps happen?

Muscle cramps occur when the normal signals between nerves and muscles become disrupted. This can be influenced by:

Changes in fluid balance (hydration)
Electrolyte levels (such as magnesium, potassium, calcium)
Muscle fatigue or overuse
Nerve sensitivity or irritation

In many cases, more than one of these factors is involved.

How is this linked to aspergillosis and its treatment?

People with aspergillosis may experience additional factors that increase the likelihood of cramps:

Medications – some treatments used in lung disease (including antifungals, corticosteroids, and inhalers) may affect muscle function or electrolyte balance
Chronic inflammation – ongoing inflammation in the body can affect muscles and nerves
Reduced activity or sudden changes in activity – both inactivity and overexertion can trigger cramps
Co-existing conditions – such as kidney or hormonal conditions, which can influence electrolyte balance

Because many patients take multiple medications, it can sometimes be difficult to identify a single cause.

Additional considerations in chronic pulmonary aspergillosis (CPA)

People living with chronic pulmonary aspergillosis (CPA) may experience additional factors that increase the likelihood of muscle cramps.

Long-term antifungal therapy – medications such as azoles (e.g. itraconazole or voriconazole) can affect electrolyte balance or interact with other medicines
Kidney function – the kidneys play a key role in regulating electrolytes, and even mild changes may contribute to cramping
Electrolyte imbalance – including magnesium, potassium, and calcium levels, which may fluctuate despite supplementation
Medication combinations – multiple treatments may have additive effects on muscles or nerves
Fatigue and reduced conditioning – common in chronic lung disease and may increase susceptibility to cramps

These factors mean that cramps in CPA are often multifactorial and may change over time.

Common Contributing Factors

Based on patient reports and clinical understanding, the following are commonly associated with muscle cramps:

Physical exertion – especially in physically demanding jobs
Age-related muscle changes
Dehydration
Electrolyte imbalance
Medication effects
Poor sleep or positioning

Some people also report cramps affecting multiple muscle groups at the same time, which can feel particularly intense.

What May Help Reduce Cramps

While individual responses vary, some general approaches that people find helpful include:

Maintaining hydration
Gentle stretching before bed
Regular, moderate activity
Medication review with a clinician or pharmacist
Balanced nutrition

Important: Supplements such as magnesium are commonly used, but may not be effective for everyone and should be discussed with a healthcare professional—particularly if you have kidney conditions or are taking multiple medications.

When to Seek Medical Advice

You should consider speaking to your GP or specialist team if:

Cramps are becoming more frequent or severe
They involve multiple muscle groups regularly
They are disrupting sleep or daily life
You have recently started or changed medications

Seek more urgent medical advice if:

Muscle weakness develops
There is swelling or redness
Dark urine or reduced urine output occurs

Common Questions

Are muscle cramps a symptom of aspergillosis?

They are not a defining symptom but are commonly reported, likely due to a combination of treatment effects and general health factors.

Why do cramps happen at night?

Night-time cramps are common and may relate to fatigue, hydration, and circulation changes during rest.

If I take magnesium, shouldn’t cramps stop?

Not necessarily. Muscle cramps often have multiple causes.

Are cramps more important to report in CPA?

Yes—particularly if you are on long-term antifungal treatment or have kidney-related issues, as these may be relevant.

References & Further Reading

National Institute for Health and Care Excellence (NICE) – Muscle cramps guidance
UK National Health Service (NHS) – Leg cramps overview
General clinical literature on electrolyte balance and muscle function

Author & Review Information

Author: Aspergillosis Patient Education Team
Review status: General educational content aligned with UK clinical practice
Disclaimer: This article is for information only and does not replace medical advice. Always consult your healthcare team regarding symptoms or treatment.

by GAtherton

How Inflammation in One Part of the Body Can Affect the Rest of the Body

Last reviewed: 24 March 2026
Audience: Patients, families, and non-specialist clinicians
Author: Aspergillosis.org editorial team

Many people think of inflammation as something that stays in one place: a painful joint, an inflamed lung, an irritated sinus, or a bowel flare. In reality, inflammation is often a whole-body process. Signals released at one site can travel through the blood, nervous system, and immune system, influencing other organs and changing how the body feels and functions overall.

This helps explain why a local health problem can sometimes lead to symptoms that seem much broader, such as fatigue, poor concentration, low mood, loss of appetite, aches, disturbed sleep, or worsening of other long-term conditions.

Key points

Inflammation is not always confined to one organ or body part.
Inflamed tissues release chemical messengers that can circulate throughout the body.
The brain, heart, kidneys, liver, gut, lungs, and immune system all communicate with one another.
This “cross-talk” can be helpful in short-term illness, but harmful when inflammation becomes prolonged.
Ongoing inflammation is linked with fatigue, brain fog, low mood, cardiovascular strain, and worsening of other chronic diseases.

What is inflammation?
Why inflammation does not always stay local
How the body communicates during inflammation
Common whole-body effects of inflammation
Why this matters in lung disease and aspergillosis
Acute inflammation versus chronic inflammation
What can help?
When to seek medical advice
Common questions
References

What is inflammation?

Inflammation is part of the body’s defence system. It is one of the ways the immune system responds to infection, injury, irritation, allergens, or tissue damage. In the short term, inflammation is often helpful. It can help the body fight infection, clear damaged tissue, and begin repair.

But inflammation can also become too strong, too prolonged, or poorly controlled. When that happens, the effects may no longer stay limited to the original problem area.

Why inflammation does not always stay local

When tissue becomes inflamed, immune cells release small signalling proteins called cytokines and other inflammatory mediators. These act like chemical messages. Some stay nearby, but many enter the bloodstream and influence distant organs.

This is why inflammation in one part of the body can sometimes cause:

tiredness or exhaustion
feeling unwell or “washed out”
poor concentration or “brain fog”
worsening appetite
sleep disruption
higher strain on the heart or kidneys
worsening of other inflammatory conditions

Researchers increasingly describe this as systemic inflammation or organ cross-talk. In other words, organs do not operate in isolation. They are part of an interconnected network.

How the body communicates during inflammation

1. Chemical messengers in the blood

Inflamed tissues can release cytokines such as interleukin-6 (IL-6), interleukin-1 beta (IL-1β), and tumour necrosis factor alpha (TNF-α). These may affect blood vessels, metabolism, the brain, the heart, and other immune cells.

These signals are useful during short-term illness, but if they remain elevated they may contribute to chronic symptoms and long-term health effects.

2. Organ-to-organ immune cross-talk

Modern immunology shows that the gut, liver, lungs, brain, heart, kidneys, and bone marrow can influence one another through immune signalling. A problem in one organ may therefore alter immune behaviour somewhere else.

This can be protective, but it can also become part of a vicious circle, especially in chronic disease.

3. Nerve signalling between the body and brain

Inflammation is not communicated only by blood. The nervous system also plays a role. Signals from inflamed tissues can travel through nerves, including the vagus nerve, to the brain. The brain then responds by adjusting immune activity and body-wide stress responses.

This helps explain why inflammation can affect fatigue, mood, motivation, sleep, and mental clarity.

4. Stress, hormones, and metabolism

Inflammation also interacts with the body’s hormonal and metabolic systems. This can influence energy use, blood sugar regulation, muscle strength, and appetite. Over time, chronic inflammation may put extra strain on the cardiovascular and kidney systems.

Common whole-body effects of inflammation

Fatigue

One of the most common effects of inflammation is fatigue. This is not simply feeling sleepy. It can be a profound lack of physical and mental energy. Many chronic inflammatory illnesses are associated with this kind of exhaustion.

Brain fog and mood changes

Inflammatory signals can affect the brain, contributing to reduced concentration, slowed thinking, low motivation, anxiety, or low mood. This does not mean symptoms are “all in the mind”. It means that immune activity can influence brain function.

Heart and blood vessel effects

Inflammation can make blood vessels less healthy over time and may contribute to a higher cardiovascular risk. This is one reason why long-standing inflammatory diseases are often linked to heart and circulatory problems.

Kidney effects

The kidneys are sensitive to inflammatory stress. In some conditions, long-term systemic inflammation can contribute to kidney damage or worsen existing kidney disease. Kidney disease itself can also increase inflammation, creating a two-way relationship.

Muscle weakness and reduced stamina

Ongoing inflammation can alter how muscles use energy and recover after activity. This may contribute to weakness, reduced exercise tolerance, and slower recovery after exertion.

Why this matters in lung disease and aspergillosis

For people with chronic lung conditions, including some forms of aspergillosis, inflammation in the airways or lungs may have effects beyond breathing alone. The lungs are not separate from the rest of the body.

Inflammation in the lungs may contribute to:

general fatigue
poor stamina
sleep disruption
brain fog
loss of appetite
worsening of other conditions

This can be especially relevant for people living with long-term inflammatory lung disease, repeated infections, allergic inflammation, or complex treatment burdens.

It is also one reason why patients sometimes feel that their symptoms are “bigger” than what would be expected from the lungs alone. Often, that experience is real and biologically plausible.

Acute inflammation versus chronic inflammation

Acute inflammation

This is the short-term response seen with infection, injury, or a sudden flare. It may cause fever, pain, swelling, and marked tiredness. Usually, it settles when the trigger is controlled.

Chronic inflammation

This is lower-grade or persistent inflammation that continues over time. It may be driven by chronic infection, immune dysregulation, ongoing tissue damage, obesity, autoimmune disease, long-term lung disease, or other medical problems. Chronic inflammation is often less dramatic but may have broader long-term effects.

What can help?

The right approach depends on the underlying cause. Broadly, management focuses on:

identifying and treating the cause of inflammation where possible
controlling infections or allergic triggers
optimising treatment of the underlying disease
supporting sleep, nutrition, and pacing of activity
monitoring the effects on other organs when relevant

There is rarely a single quick fix for chronic inflammation. Good management usually means looking at the whole person, not just the inflamed organ.

When to seek medical advice

Please seek medical advice if inflammation-related symptoms are worsening or if you develop:

new or severe breathlessness
chest pain
confusion or marked drowsiness
new swelling, reduced urine output, or signs of dehydration
persistent fevers
rapid decline in energy, mobility, or daily functioning

If symptoms are sudden, severe, or alarming, seek urgent medical help.

Common questions

Does inflammation always damage the whole body?

No. Short-term, controlled inflammation is a normal and useful response. Problems are more likely when inflammation is severe, repeated, or persistent.

Can one inflamed organ affect another?

Yes. There is now strong evidence that organs influence one another through immune, vascular, metabolic, and nerve-based pathways.

Can inflammation cause fatigue even if blood tests are not dramatically abnormal?

Yes. Symptoms and blood markers do not always match perfectly. Some people experience substantial fatigue and other systemic symptoms even when routine blood tests are only mildly abnormal or intermittently raised.

Is this relevant to chronic lung disease?

Yes. Lung inflammation can have effects that go beyond breathing, including fatigue, reduced stamina, and wider body effects.

References

Dou J, et al. The Interplay of Cross-Organ Immune Regulation in Inflammation and Cancer. MedComm. 2025.
Jin H, Li M, et al. A body–brain circuit that regulates body inflammatory responses. Nature. 2024.
Katkenov N, et al. Systematic Review on the Role of IL-6 and IL-1β in Cardiovascular Diseases. Journal of Cardiovascular Development and Disease. 2024.
Nowak KL, et al. Targeting Inflammation in CKD. Current Opinion in Nephrology and Hypertension. 2025.
Paganin W, et al. Inflammatory biomarkers in depression: a scoping review. 2024.
Mehta NN, et al. IL-6 and Cardiovascular Risk: A Narrative Review. 2024.
Che H, et al. Organ cross-talk: molecular mechanisms, biological functions and therapeutic opportunities. 2026.

Disclaimer: This article is for general information and education. It is not a substitute for personalised medical advice. If you are worried about worsening symptoms, new symptoms, or the effect of inflammation on your health, speak to your clinical team.

by GAtherton

Managing fatigue and energy in aspergillosis and allergic fungal lung disease

Key points

Many people with aspergillus-related lung conditions experience extreme tiredness after physical or mental exertion.
This fatigue can last hours or even several days.
Breathing, immune activity, inflammation and sometimes hormone imbalance all use extra energy.
Activity can temporarily increase airway inflammation and mucus.
Managing energy carefully (“spoon theory”) can help prevent fatigue crashes.

Why people with lung disease feel exhausted after exertion
What is happening in the lungs and body
Managing energy: the “spoon theory”
Practical ways to manage energy
Nutrition and adrenal health
Warning signs you are running out of energy
Why fatigue in lung disease is different from normal tiredness
Daily energy management checklist
Can this fatigue be treated?

When to talk to your doctor

Why people with lung disease feel exhausted after exertion

Healthy lungs have a large reserve capacity. When we exercise or do physical work, breathing becomes deeper and faster, but the lungs can usually cope easily.

In people with aspergillosis or allergic airway disease, the airways may already be:

inflamed
narrowed
filled with mucus
sensitive to allergens such as Aspergillus fumigatus

When the body demands more oxygen during activity, the lungs must work much harder to supply it. Activities that seem minor to other people may therefore require much greater effort from the body.

What is happening in the lungs and body?

Inflamed airways

Many aspergillus-related conditions involve inflammation in the airways. The immune system releases chemicals that cause:

swelling of airway walls
increased mucus production
greater airway sensitivity

During exertion, breathing becomes faster and deeper, which can irritate these inflamed airways further.

Mucus affecting airflow

Inflamed airways often produce extra mucus. This mucus can partly block airflow and lead to:

coughing
wheezing
breathlessness
uneven airflow within the lungs

This may reduce how efficiently oxygen enters the bloodstream. Doctors sometimes refer to this as ventilation–perfusion mismatch.

Breathing uses more energy

In healthy people, breathing uses only a small fraction of the body's energy. In lung disease, breathing may require much more effort.

Additional muscles may assist breathing, including:

chest muscles
neck muscles
shoulder muscles

These muscles can become fatigued during activity, just like leg muscles after exercise.

Immune system activity

If the immune system reacts to fungal proteins or allergens, it releases signalling chemicals called cytokines. These chemicals can produce symptoms similar to mild illness, including fatigue, brain fog and muscle aches.

Delayed inflammation after activity

Some people notice that fatigue appears later rather than immediately. Physical effort can trigger inflammation that develops over 12–48 hours, increasing mucus production, airway irritation and tiredness.

This explains why people sometimes feel worse the day after a busy day.

Managing energy: the “spoon theory”

Many people with chronic illness find it helpful to think about their energy using the idea of spoon theory.

In this idea:

each spoon represents a small unit of energy
you start the day with a limited number of spoons
each activity uses some of those spoons

Because breathing and inflammation already use energy, people with lung disease may begin the day with fewer spoons available.

Example of spoon use

Activity	Possible energy use
Getting dressed	1 spoon
Showering	2–3 spoons
Cooking a meal	2 spoons
Doctor’s appointment	3–4 spoons
Busy social day	Many spoons

If too many spoons are used early in the day, the body may run out of energy, leading to exhaustion lasting hours or even days.

Practical ways to manage energy

Plan activities around your best time of day

Time of day	Suggested activities
Morning	Errands or appointments
Midday	Light household tasks
Afternoon	Quieter activities
Evening	Rest and recovery

Break tasks into smaller steps

Large tasks can overwhelm the lungs and muscles. Instead of doing everything at once:

clean one room at a time
cook in stages
prepare things earlier in the day

Use the 50–70% rule

Try to stop activity when you reach about half to two-thirds of your limit. Stopping early often prevents the fatigue crash that can occur later.

Use breathing techniques

Pursed-lip breathing

breathe in through your nose
breathe out slowly through gently pursed lips

Rhythmic breathing

Match breathing with movement, for example when climbing stairs.

Keep mucus moving

Mucus increases the work of breathing. Helpful strategies include:

airway clearance techniques
staying well hydrated
gentle movement
using inhalers or nebulisers as prescribed

Maintain gentle regular activity

Although exertion can cause fatigue, complete inactivity can worsen the problem. Gentle activity such as walking or pulmonary rehabilitation exercises helps maintain muscle strength.

Protect sleep

maintain a regular sleep routine
clear mucus before bedtime if needed
avoid heavy exertion late in the evening

Nutrition and adrenal health

Nutrition and energy

Good nutrition helps support energy levels. Helpful strategies include:

eating regular meals
including protein for muscle repair (eggs, fish, dairy, beans or nuts)
eating complex carbohydrates for steady energy
drinking enough fluids

Some people find that smaller, more frequent meals reduce breathlessness compared with large meals.

Important nutrients

protein
vitamin D
iron
B vitamins

Doctors may check for deficiencies if fatigue is severe.

Adrenal insufficiency

Some patients who have taken long-term steroid medications may develop adrenal insufficiency. The adrenal glands normally produce cortisol, which helps regulate energy and stress responses.

Symptoms may include:

severe fatigue
dizziness
muscle weakness
difficulty recovering after exertion

Patients with adrenal insufficiency usually take hydrocortisone replacement therapy and should follow their doctor’s advice carefully.

Warning signs you are running out of energy

breathing becomes faster or more difficult
increased coughing or mucus
arms or legs feel heavy
dizziness or weakness
difficulty concentrating
chest tightness or wheezing

When these warning signs appear, it is usually best to stop and rest before continuing.

Why fatigue in lung disease is different from normal tiredness

Fatigue in lung disease is not simply normal tiredness. Several factors occur at the same time:

breathing requires more energy
the immune system may be active
oxygen exchange may be less efficient
nutrition and hormone balance may influence recovery

Because of this combination, fatigue may appear suddenly and last longer than expected.

Daily energy management checklist

Pacing and activity

spread activities across the day
stop before exhaustion
plan demanding tasks when energy is highest
allow recovery time after busy days

Breathing and airway care

use breathing techniques during exertion
perform airway clearance if needed
take inhalers or nebulisers as prescribed
stay well hydrated

Nutrition and medication

eat regular meals
include protein for muscle strength
take medications as prescribed
follow sick-day rules if you have adrenal insufficiency

Sleep and recovery

maintain a regular sleep routine
clear mucus before bedtime
rest when warning signs appear

Can this fatigue be treated?

Fatigue associated with aspergillosis, allergic fungal airway disease, or severe asthma can sometimes be improved when the underlying causes are treated. Because several different processes contribute to fatigue, treatment usually focuses on improving multiple factors rather than a single cure.

Treating airway inflammation

Inflammation in the airways is one of the major contributors to fatigue. When the airways are inflamed:

breathing requires more effort
mucus production increases
oxygen exchange becomes less efficient

Treatments aimed at reducing airway inflammation may include:

Inhaled corticosteroids – commonly used in asthma to reduce inflammation directly in the airways.
Antifungal therapy – in some patients, reducing fungal growth can reduce immune activation and inflammation.
Biologic therapies – newer treatments that target specific immune pathways involved in allergic and inflammatory lung disease.

Biologic treatments

Biologics are one of the most promising areas of treatment for severe asthma and allergic airway disease. These medications target specific parts of the immune system that drive inflammation.

Biologic	Target	Effect
Omalizumab	IgE	Reduces allergic inflammation
Mepolizumab / Benralizumab	IL-5 pathway	Reduces eosinophilic inflammation
Dupilumab	IL-4 / IL-13	Reduces type-2 inflammation
Tezepelumab	TSLP	Blocks upstream inflammatory signalling

Some patients with conditions such as allergic bronchopulmonary aspergillosis (ABPA) or severe asthma report improvements in breathlessness, symptoms and overall energy levels when inflammation is better controlled.

Improving mucus clearance

Mucus in the airways increases the work of breathing and can contribute to fatigue. Strategies that may help include:

airway clearance techniques
physiotherapy
maintaining good hydration
using prescribed inhalers or nebulisers correctly

Treating other contributing factors

Fatigue can also be worsened by other health issues that are common in chronic lung disease, such as:

iron deficiency
vitamin deficiencies
poor sleep
adrenal insufficiency
muscle deconditioning

Addressing these factors can sometimes improve overall energy levels.

Pulmonary rehabilitation

Pulmonary rehabilitation programmes combine exercise training, breathing techniques and education about pacing activities. These programmes can improve muscle efficiency and exercise tolerance, and many patients report reduced fatigue and improved quality of life.

Future treatments

Research into inflammatory lung diseases is advancing rapidly. New biologic drugs and other targeted therapies are being developed that may improve control of airway inflammation.

Researchers are also studying how the lung microbiome (bacteria and fungi living in the airways) influences inflammation. In the future, this may lead to more personalised treatments for patients with fungal-related lung disease.

Inflammatory fatigue

Researchers are increasingly recognising that chronic inflammatory diseases can cause a form of fatigue sometimes called “inflammatory fatigue.”

In these conditions, immune signalling chemicals released during inflammation can affect the brain and energy metabolism. Similar patterns of fatigue are seen in diseases such as rheumatoid arthritis and inflammatory bowel disease.

This may help explain why some treatments that reduce inflammation — including biologic therapies — can improve fatigue even when lung function measurements change only modestly.

Interrupting the fatigue cycle

Treatment aims to interrupt the cycle that can develop in chronic lung disease:

Airway inflammation
↓
Breathing requires more effort
↓
More energy used by respiratory muscles
↓
Immune system activity
↓
Reduced overall energy and fatigue

By improving airway inflammation, mucus clearance, muscle strength and overall health, many patients find their energy levels become more manageable.

When to talk to your doctor

Seek medical advice if:

fatigue becomes progressively worse
breathlessness increases
new symptoms appear such as chest pain or coughing up blood
fatigue prevents normal daily activities

A reassuring message

Many people with aspergillosis or allergic airway disease worry that exhaustion means their condition is worsening.

In most cases it reflects the extra energy required for breathing, inflammation and immune activity. Learning to pace activity can help people live more comfortably with chronic lung disease.

Author: National Aspergillosis Centre information team
Review: Clinical review recommended
Last reviewed: 2026

by GAtherton

Nontuberculous Mycobacteria (NTM–MAC) and Aspergillosis

Why these infections sometimes occur together

Audience: Aspergillosis patients, carers, GPs and non-specialist clinicians

Some patients with Allergic Bronchopulmonary Aspergillosis (ABPA) may be investigated for nontuberculous mycobacteria (NTM), because airway damage from ABPA can increase susceptibility to other lung infections.

Key points

Nontuberculous mycobacteria (NTM) are environmental bacteria that sometimes infect damaged lungs.
The most common NTM causing lung disease is the Mycobacterium avium complex (MAC).
NTM infection and aspergillosis often occur in the same patients because both thrive in damaged airways such as bronchiectasis or lung cavities.
Some patients with ABPA are investigated for NTM because ABPA can lead to bronchiectasis and impaired mucus clearance.
NTM infections usually grow very slowly, so treatment is sometimes monitored rather than started immediately.
Treating NTM and aspergillosis together can be difficult because some NTM antibiotics interfere with antifungal medicines.
Doctors usually treat the infection causing the most harm first while monitoring the other carefully.

What are NTM?
What is Mycobacterium avium complex (MAC)?
Why NTM infections occur in some people
What is bronchiectasis?
Why patients with ABPA may be asked about NTM
Why NTM and Aspergillus infections often occur together
The lung infection cycle
Chronic lung disease as a microbial ecosystem
Why treatment can be complicated
When treatment for NTM may be delayed
How doctors balance treatment decisions
NTM vs Aspergillosis – comparison table
Common questions patients ask about NTM and Aspergillus
When should patients seek medical advice?
Reducing exposure to NTM in the environment

What are nontuberculous mycobacteria (NTM)?

Nontuberculous mycobacteria (NTM) are bacteria found naturally in the environment.

They live in:

soil
water
dust
plumbing systems
shower heads and taps

Unlike tuberculosis, these bacteria are not normally spread between people.

Most people inhale them regularly without becoming ill. However, in some people with damaged lungs, these bacteria can establish a long-term lung infection.

What is Mycobacterium avium complex (MAC)?

The Mycobacterium avium complex (MAC) is the most common cause of NTM lung disease.

This group includes:

Mycobacterium avium
Mycobacterium intracellulare

MAC lung disease usually develops slowly over months or years.

Symptoms may include:

chronic cough
sputum production
breathlessness
fatigue
weight loss

Because symptoms develop gradually, diagnosis can sometimes take time.

Why NTM infections occur in some people

NTM infections usually develop in people who already have structural lung disease.

Examples include:

bronchiectasis
chronic obstructive pulmonary disease (COPD)
cystic fibrosis
previous tuberculosis
severe asthma
aspergillosis

In these conditions, the lungs have damaged or widened airways, making it harder to clear mucus and microbes.

What is bronchiectasis?

Bronchiectasis is a condition where the airways become permanently widened and distorted.

In healthy lungs, mucus is cleared using:

mucus movement
tiny hair-like structures called cilia
coughing

In bronchiectasis:

mucus collects in the airways
microbes become trapped
infections become more likely

Bronchiectasis is common in patients with Allergic Bronchopulmonary Aspergillosis (ABPA) and other chronic lung diseases.

Why patients with ABPA may be asked about NTM

Some patients with Allergic Bronchopulmonary Aspergillosis (ABPA) are surprised when their doctors start investigating nontuberculous mycobacteria (NTM).

This usually happens because ABPA can lead to bronchiectasis, which increases the risk of other lung infections.

In ABPA:

inflammation caused by allergic reactions to Aspergillus can damage the airways
over time the airways may become widened and distorted, causing bronchiectasis
mucus clearance becomes less effective

When mucus accumulates in the airways, microbes that are normally cleared from the lungs can sometimes persist. These may include:

nontuberculous mycobacteria (NTM)
Pseudomonas bacteria
other organisms that affect bronchiectasis patients

For this reason, doctors sometimes test patients with ABPA for NTM if:

CT scans show bronchiectasis or nodules
sputum cultures repeatedly grow unusual organisms
symptoms worsen without a clear explanation

Importantly, having ABPA does not mean you will develop NTM infection. Most patients with ABPA never develop NTM disease.

However, because the conditions share similar risk factors, doctors sometimes check for both.

Why NTM and Aspergillus infections often occur together

NTM bacteria and Aspergillus fungi both thrive in damaged lungs.

Three factors explain the overlap.

1. Damaged airways trap microbes

When airways are widened or distorted:

mucus collects
microbes are not cleared effectively

This allows organisms such as NTM and Aspergillus to persist.

2. Chronic infection causes further lung damage

NTM infection can lead to:

inflammation
worsening bronchiectasis
lung nodules
sometimes lung cavities

These cavities can then be colonised by Aspergillus, which may lead to chronic pulmonary aspergillosis (CPA).

3. Aspergillus can worsen structural damage

Once Aspergillus becomes established it can cause:

inflammation
enlargement of lung cavities
worsening bronchiectasis

This further damage makes the lungs even more susceptible to infection.

The lung infection cycle

In many patients the relationship between bronchiectasis, NTM and Aspergillus becomes a cycle:

Lung disease develops
Bronchiectasis forms
NTM infection establishes
Lung damage worsens
Aspergillus colonises damaged tissue
Chronic aspergillosis develops
Lung damage continues

At this stage the lungs may contain multiple organisms simultaneously.

Chronic lung disease as a microbial ecosystem

Doctors increasingly recognise that damaged lungs may contain several interacting microbes rather than a single infection.

Common organisms include:

Mycobacterium avium complex (MAC)
Aspergillus species
Pseudomonas bacteria
other organisms

For this reason clinicians sometimes describe chronic lung disease as a disturbed lung microbial ecosystem.

Why treatment can be complicated

NTM and aspergillosis treatments can interact.

Typical MAC treatment includes:

azithromycin or clarithromycin
ethambutol
rifampicin

However rifampicin strongly reduces levels of antifungal drugs, including:

itraconazole
voriconazole
posaconazole

These antifungals are commonly used to treat chronic pulmonary aspergillosis.

Because of this interaction, treating both infections at the same time can be challenging.

Other medicines that may interact with rifampicin

Rifampicin affects how the liver processes many medicines. This means it can reduce the effectiveness of several commonly used drugs, including some treatments for heart conditions, blood thinners, hormonal medicines, and certain antidepressants.

Because of this, doctors and pharmacists always review a patient’s medication list before starting rifampicin. Patients should tell their healthcare team about all medicines they take, including over-the-counter medicines, inhalers, and herbal supplements. In most cases, safe alternatives or dose adjustments can be used if needed.

When treatment for NTM may be delayed

Unlike many bacterial infections, MAC often progresses slowly.

Doctors sometimes monitor the infection before starting treatment. This approach is called active monitoring or watchful waiting.

Monitoring may include:

CT scans
sputum cultures
lung function tests
symptom assessment

Treatment may be delayed if:

symptoms are mild
CT scans are stable
another condition requires more urgent treatment

For example, aspergillosis may be treated first if it is causing the main symptoms or lung damage.

How doctors balance treatment decisions

When both infections are present, clinicians try to identify which infection is currently causing the most harm.

Doctors consider:

Symptoms

worsening cough
breathlessness
fatigue
weight loss
haemoptysis (coughing blood)

CT scan findings

enlarging cavities
fungal balls
nodules typical of NTM disease
worsening bronchiectasis

Laboratory results

sputum cultures for NTM
Aspergillus blood tests, such as Aspergillus IgG

If one infection clearly explains the patient’s symptoms, that infection usually becomes the treatment priority.

Treatment plans may then change over time as the balance of disease changes.

NTM vs Aspergillosis – What’s the difference?

Feature	NTM (MAC) Lung Disease	Aspergillosis
Type of organism	Bacteria	Fungus
Source	Soil, water, plumbing	Airborne fungal spores
Spread between people	Rare	Does not spread
Typical speed	Slow, chronic infection	Variable
Typical CT findings	Nodules, bronchiectasis, cavities	Cavities, fungal balls, airway inflammation
Treatment	Long antibiotic courses, often 12–18 months	Antifungal medicines
Drug interaction issues	Rifampicin interferes with antifungals	Antifungal levels can be reduced by rifampicin

Common questions patients ask about NTM and Aspergillus

If MAC grows slowly, why treat it?

Although MAC grows slowly, it can still cause progressive lung damage over time.

Treatment is usually recommended if there is:

worsening symptoms
declining lung function
progressive CT scan changes

Can NTM be present without causing disease?

Yes. Some people have NTM colonisation without active infection.

Doctors diagnose NTM lung disease only when symptoms, imaging findings and repeated cultures all support the diagnosis.

Why do NTM and Aspergillus often occur together?

Both organisms tend to grow in damaged airways, especially where bronchiectasis is present and mucus clearance is poor.

Will both infections always be treated?

Not necessarily. Doctors often treat the infection causing the most immediate problem while monitoring the other.

Does NTM mean my aspergillosis is worsening?

Not necessarily. Both infections occur in damaged lungs, so they may simply share the same environment.

Can NTM lead to aspergillosis?

Sometimes. If NTM infection causes lung cavities or worsening bronchiectasis, these damaged areas may later become colonised by Aspergillus.

Should I worry if my doctor decides not to treat NTM immediately?

Not necessarily. Because MAC often progresses slowly, doctors sometimes choose active monitoring rather than immediate treatment.

When should patients seek medical advice?

People living with aspergillosis, bronchiectasis or NTM infection often have ongoing symptoms such as cough and sputum production. These symptoms may fluctuate and do not always mean the disease is worsening.

However, certain changes should prompt medical review.

Seek medical advice if you notice worsening breathing symptoms

increasing breathlessness
a significant increase in cough
a noticeable increase in sputum production
sputum becoming thicker, darker or foul-smelling

These symptoms may indicate:

bacterial infection
worsening bronchiectasis
progression of NTM infection
worsening aspergillosis

Coughing up blood (haemoptysis)

Haemoptysis can occur in both bronchiectasis and aspergillosis.

Seek medical advice if:

bleeding increases
blood appears repeatedly
there is more than a small amount of blood
bleeding occurs suddenly with breathlessness

Large amounts of blood should be treated as a medical emergency.

Unexplained weight loss or increasing fatigue

Persistent or worsening:

weight loss
fatigue
loss of appetite

may indicate:

progressive infection
increasing inflammation
advancing NTM disease

Fever or feeling unwell

New symptoms such as:

fever
chills
chest discomfort
feeling generally unwell

may suggest a new infection, such as a bacterial chest infection, which may require treatment.

Rapid change in symptoms

Seek medical advice if you experience:

sudden worsening breathlessness
significant chest pain
new wheezing
severe fatigue developing quickly

Symptoms that may remain stable

Many people with chronic lung disease experience symptoms that remain relatively stable for long periods, including:

a chronic cough
daily sputum production
mild breathlessness
intermittent fatigue

Doctors monitor these symptoms over time using:

CT scans
sputum cultures
lung function tests

These investigations help clinicians determine whether infections such as NTM or Aspergillus are stable or progressing.

Reducing exposure to NTM in the environment

Patients with bronchiectasis, ABPA, or other chronic lung diseases sometimes ask whether they should try to avoid environmental exposure to nontuberculous mycobacteria (NTM).

NTM are very common in the natural environment and cannot be completely avoided. They are found in:

soil and compost
garden dust
natural water sources
tap water and plumbing systems
showerheads
hot tubs and spa pools

For most people, the goal is sensible risk reduction rather than strict avoidance. Major lifestyle restrictions are usually not necessary.

Water exposure

NTM can grow in biofilms inside plumbing systems, including showerheads. Small amounts of bacteria may become airborne when water is aerosolised.

Some simple precautions may help reduce exposure:

avoid frequent use of hot tubs or spa pools
allow taps or showers to run briefly if they have not been used for several days
clean showerheads periodically to remove biofilm and limescale

Normal showering and bathing are considered safe for most patients.

NTM infection occurs when bacteria are inhaled into the lungs rather than swallowed. Drinking ordinary tap water is therefore considered safe for most people, and patients are not usually advised to avoid tap water for drinking.

Gardening and soil exposure

NTM bacteria are often present in soil and compost. Gardening can still be enjoyed safely with a few sensible precautions.

wear gloves when gardening
avoid inhaling dust from dry compost or soil
dampen compost before handling to reduce dust
wash hands after gardening

For people with bronchiectasis or NTM disease, wearing a mask during dusty gardening activities may help reduce inhalation of soil particles.

Reducing dust exposure

Activities that generate dust can increase inhalation of environmental microbes.

Helpful precautions include:

avoiding sweeping very dusty areas indoors
ventilating indoor spaces
wearing a mask during dusty tasks such as handling compost or dry soil

Cleaning showerheads

Cleaning showerheads periodically can help remove limescale and biofilms where microbes may grow.

A simple method is:

Remove the showerhead if possible.
Soak it in white vinegar for about 30–60 minutes.
Gently scrub the spray holes with a small brush.
Rinse thoroughly.
Run hot water for 30–60 seconds before use.

If the showerhead cannot be removed, a plastic bag filled with vinegar can be tied around the head so that it soaks.

Cleaning every 1–3 months is usually sufficient.

What is usually not necessary

Experts generally do not recommend major lifestyle changes to avoid NTM exposure. In most cases it is not necessary to:

avoid showers
avoid gardening completely
install specialised water filtration systems

These activities are important for quality of life and general health, and evidence that strict avoidance prevents NTM disease is limited.

The most important protection

For patients with ABPA, bronchiectasis or aspergillosis, the most important protective measures remain:

good airway clearance
regular medical monitoring
prompt treatment of infections
maintaining overall lung health

Reducing environmental exposure may help slightly, but good management of lung disease remains the most important factor.

Key message

When NTM and Aspergillus infections occur together, treatment decisions focus on which infection is currently causing the most damage, while avoiding harmful drug interactions.

For patients with ABPA, one reason NTM may be discussed is that ABPA can lead to bronchiectasis and impaired mucus clearance, which can make other infections more likely.

Many patients live with these conditions for years with careful monitoring and specialist management.

Author: National Aspergillosis Centre Patient Information Team
Last reviewed: March 2026

by GAtherton

Asthma and Aspergillosis

How fungal spores interact with asthma and other lung diseases

Every day we inhale thousands of microscopic fungal spores from the environment. One of the most common fungi in the air is Aspergillus fumigatus. In healthy lungs these spores are removed quickly by the lungs’ natural defence systems and cause no illness.

However, in people with asthma—particularly severe asthma—the interaction between the lungs and Aspergillus can be very different. The fungus may trigger allergic inflammation, grow in mucus within the airways, or occasionally contribute to chronic lung disease.

Understanding this relationship helps explain several important conditions including:

Aspergillus sensitisation
Severe Asthma with Fungal Sensitisation (SAFS)
Allergic Bronchopulmonary Aspergillosis (ABPA)
Aspergillus bronchitis
Chronic Pulmonary Aspergillosis (CPA)

Although asthma is the most common condition linked to Aspergillus allergy, other lung diseases such as bronchiectasis, Chronic Obstructive Pulmonary Disease (COPD), and tuberculosis-related lung damage can also create environments where the fungus becomes important.

Why Asthma Creates a Favourable Environment for Aspergillus

Asthma is a disease of airway inflammation and hyper-reactivity. The bronchi narrow during attacks because the airway wall becomes swollen and the surrounding smooth muscle contracts.

Several features of asthma make it easier for Aspergillus spores to remain in the lungs.

Mucus production

Asthma often causes increased production of thick airway mucus.

Normally mucus traps inhaled particles and moves them upward toward the throat via the mucociliary escalator.

In asthma:

mucus becomes thicker
clearance becomes less efficient
spores remain trapped

This trapped environment allows fungal spores to persist in the airway mucus.

Allergic immune responses

Many asthma patients have Type-2 (T2) inflammation (50-70%), involving immune pathways driven by:

Immunoglobulin E (IgE)
Interleukin-4
Interleukin-5
Interleukin-13
eosinophils

These pathways respond strongly to fungal allergens. When the immune system recognises Aspergillus proteins it may trigger allergic inflammation in the airways.

Fungal sensitisation is increasingly recognised as an important contributor to severe asthma (PMID: 24735832).

Aspergillus Sensitisation

Many people with asthma develop allergic sensitisation to Aspergillus.

Sensitisation means the immune system produces antibodies against fungal proteins.

Features include:

positive Aspergillus skin test or IgE blood test
worsening asthma symptoms
increased exacerbations

Studies suggest 10–25% of patients attending severe asthma clinics show Aspergillus sensitisation (PMID: 24735832).

However, sensitisation alone does not necessarily cause lung damage.

Severe Asthma with Fungal Sensitisation (SAFS)

Some patients with severe asthma have fungal sensitisation but do not meet the criteria for ABPA.

This condition is known as Severe Asthma with Fungal Sensitisation (SAFS).

Typical features include:

severe or poorly controlled asthma
fungal allergy
moderate IgE elevation

A randomised controlled trial demonstrated that antifungal therapy may improve symptoms in some SAFS patients (PMID: 18948425).

Allergic Bronchopulmonary Aspergillosis (ABPA)

Allergic Bronchopulmonary Aspergillosis is the most important Aspergillus-related disease associated with asthma.

ABPA occurs when Aspergillus grows within airway mucus and triggers a strong allergic immune response.

Typical findings include:

very high total IgE levels
Aspergillus-specific IgE and IgG antibodies
eosinophilia
mucus plugs containing fungal hyphae
central bronchiectasis

ABPA occurs in approximately:

1–2% of all asthma patients
up to 10–15% of severe asthma patients

These figures come from global prevalence estimates of ABPA in asthma populations (PMID: 23210682/.

Modern diagnostic criteria for ABPA were updated by the International Society for Human and Animal Mycology (ISHAM) in 2024 (PMID: 38423624).

Asthma and Aspergillus Disease Pathway

Possible interactions between asthma and Aspergillus. Some patients develop allergic disease (ABPA) which may lead to airway damage such as bronchiectasis (NB Progression to CPA is very rare).

When ABPA Causes Bronchiectasis

Repeated inflammation from ABPA may damage airway walls and lead to bronchiectasis.

Bronchiectasis occurs when airways become:

permanently widened
distorted
unable to clear mucus effectively

Instead of being cleared from the lungs, mucus pools in the airways.

This retained mucus creates an environment where microorganisms—including fungi—can grow.

Aspergillus Bronchitis

In some patients with bronchiectasis or chronic lung disease, Aspergillus may persist in airway mucus and cause chronic airway infection rather than allergy.

Symptoms may include:

chronic cough
sputum production
repeated positive Aspergillus cultures

IgE levels are usually lower than in ABPA.

Chronic Pulmonary Aspergillosis (CPA)

Chronic Pulmonary Aspergillosis is a slowly progressive fungal infection of damaged lung tissue.

CPA usually develops in lungs containing:

cavities
severe structural damage

Common underlying diseases include:

tuberculosis
sarcoidosis
severe COPD

Globally, the most common cause of CPA is previous tuberculosis infection (PMID: 22271943).

Asthma alone rarely causes CPA, but severe bronchiectasis or ABPA-related lung damage may occasionally lead to it.

Aspergillosis and Immune Competence

Different forms of aspergillosis occur depending on lung damage and immune function.

Key Messages

Asthma is one of the most important diseases associated with Aspergillus-related lung conditions.
Many asthma patients develop fungal sensitisation.
A smaller proportion develop Allergic Bronchopulmonary Aspergillosis (ABPA).
Repeated inflammation from ABPA can lead to bronchiectasis.
Chronic pulmonary aspergillosis is rare in asthma alone but may occur if significant lung damage develops.

Understanding these interactions helps guide diagnosis and treatment for people living with asthma and Aspergillus-related disease.

Bronchiectasis in Aspergillosis Patients

Many people with aspergillosis also develop bronchiectasis, a condition in which some of the airways in the lungs become permanently widened and damaged. Understanding bronchiectasis can help explain many symptoms experienced by patients with Allergic Bronchopulmonary Aspergillosis (ABPA – Allergic Bronchopulmonary Aspergillosis) and Chronic Pulmonary Aspergillosis (CPA – Chronic Pulmonary Aspergillosis).

Although bronchiectasis cannot usually be reversed, it can often be managed effectively, and understanding how it works helps patients recognise symptoms and flare-ups early.

The airways of the lungs

Your lungs contain a branching network of tubes called bronchi and bronchioles that carry air in and out of the lungs.

Air travels through the trachea (windpipe) into the bronchi, which then divide repeatedly into smaller and smaller tubes called bronchioles. At the ends of the bronchioles are millions of tiny air sacs called alveoli, where oxygen moves into the bloodstream.

The lining of the airways produces a thin layer of mucus that traps dust, bacteria and fungal spores that we breathe in every day.

Tiny hair-like structures called cilia move this mucus upward toward the throat, where it can be swallowed or coughed out. This system acts like a self-cleaning escalator, helping keep the lungs clear.

What is bronchiectasis?

In bronchiectasis, some of the airways become permanently widened and damaged.

When this happens:

the airway walls become inflamed and weakened
the tubes widen and lose their normal shape
mucus becomes harder to clear
bacteria and fungi can grow in trapped mucus

Over time, this leads to repeated infections and inflammation.

Doctors often describe bronchiectasis as a vicious cycle:

Infection or inflammation damages the airway
The airway widens and mucus clearance becomes poor
Mucus builds up in the airway
Bacteria and fungi grow in the mucus
Infection and inflammation occur again

Without treatment, this cycle can gradually worsen airway damage.

Why bronchiectasis is common in aspergillosis

Bronchiectasis is particularly common in patients with aspergillosis, especially in ABPA.

In ABPA, the immune system reacts strongly to Aspergillus spores in the airways. This causes:

allergic inflammation in the bronchi
thick mucus plugs
repeated airway irritation

Over time, this inflammation can damage the airway walls and lead to bronchiectasis, often affecting the central airways of the lungs.

Once bronchiectasis develops, mucus becomes harder to clear, which can allow bacteria and fungi such as Aspergillus to persist in the lungs.

Symptoms of bronchiectasis

Many symptoms of bronchiectasis overlap with those of aspergillosis.

Common symptoms include:

persistent cough
regular sputum (phlegm) production
breathlessness
fatigue
frequent chest infections

Sputum may be:

clear
yellow or green
occasionally blood-streaked

In people with ABPA, patients sometimes cough up thick mucus plugs, which may appear brown or rubbery.

How bronchiectasis is diagnosed

Bronchiectasis is usually diagnosed using a High Resolution CT (HRCT) scan of the lungs.

On a CT scan, doctors may see:

widened airways
thickened airway walls
mucus plugs
airways extending closer to the edge of the lung than normal

Radiologists sometimes describe a typical appearance called the “signet ring sign”, where the widened airway appears larger than the nearby blood vessel.

Bronchiectasis and aspergillosis flare-ups

Because bronchiectasis and aspergillosis affect the same airways, it can sometimes be difficult for patients to recognise whether worsening symptoms are caused by:

a bronchiectasis infection, or
an aspergillosis flare-up.

Understanding the differences can help patients recognise when to seek medical advice.

Bronchiectasis exacerbations

Bronchiectasis flare-ups are usually caused by bacterial infection in trapped mucus.

Patients may notice:

increased sputum production
sputum becoming yellow or green
increased coughing
fever or feeling unwell
breathlessness

Many patients describe bronchiectasis exacerbations as feeling like a chest infection.

Treatment usually involves:

antibiotics
airway clearance physiotherapy
increased mucus clearance

Aspergillosis flare-ups

Aspergillosis flare-ups are usually caused by fungal activity or immune reactions to Aspergillus.

Patients may notice:

worsening wheezing
chest tightness
increased breathlessness
thick mucus plugs

Some patients cough up:

brown mucus
rubbery mucus plugs
mucus shaped like small airway casts

In Chronic Pulmonary Aspergillosis, patients may also experience:

persistent cough
fatigue
weight loss
occasionally coughing blood

Treatment may involve:

steroid treatment
antifungal medication
biologic therapies in ABPA

Key differences patients often notice

Feature	Bronchiectasis flare-up	Aspergillosis flare-up
Main cause	Bacterial infection in trapped mucus	Fungal activity or immune reaction to Aspergillus
Sputum colour	Yellow or green	Brown mucus plugs or thick sticky mucus
Fever	More common	Less common
Wheezing	Sometimes present	Often worse
Feeling like a chest infection	Common	Less typical
Response to antibiotics	Usually improves	Usually little improvement
Mucus plugs	Less common	More common in ABPA
Blood tests	Usually unchanged	IgE may rise in ABPA

Both conditions can occur together

In reality, bronchiectasis and aspergillosis often interact with each other.

For example:

ABPA can cause bronchiectasis
bronchiectasis allows fungi and bacteria to remain in mucus
infection and fungal inflammation can occur at the same time

Doctors may investigate flare-ups using:

sputum cultures
blood tests (for example IgE levels in ABPA)
CT scans
inflammatory markers

Why airway clearance is important

Because bronchiectasis makes mucus harder to clear, airway clearance physiotherapy becomes a key part of treatment.

Common techniques include:

Active Cycle of Breathing Technique (ACBT)
Autogenic drainage
oscillating devices such as Flutter or Acapella

Regular airway clearance helps:

remove mucus from the lungs
reduce infections
improve breathing
reduce cough

For patients with aspergillosis, clearing mucus may also help remove fungal material from the airways.

When patients should seek medical advice

Patients should contact their healthcare team if they notice:

rapidly increasing sputum
fever or feeling unwell
coughing blood
severe breathlessness
large mucus plugs

Early treatment can often prevent a mild flare-up from becoming a more serious infection.

The key message

Bronchiectasis means that some airways in the lungs have become permanently widened, making mucus harder to clear.

However, many people with aspergillosis and bronchiectasis live active lives with stable lung function.

With good treatment, airway clearance, and early management of infections, bronchiectasis can often be well controlled for many years.

by GAtherton

Antifungal Medicines: Dosing, Monitoring, and the Role of Specialist Care

A detailed reference for patients and non-specialist clinicians

1. Why antifungal treatment is different from most medicines

Oral antifungal medicines—especially azole antifungals—are essential for treating long-term fungal diseases such as chronic pulmonary aspergillosis and allergic bronchopulmonary aspergillosis.

They differ from many common medicines because they:

Have a narrow margin between effectiveness and toxicity
Behave very differently between individuals
Are often taken for months or years, not days
Interact with many commonly prescribed drugs

For these reasons, antifungal treatment requires individualised dosing, monitoring, and specialist input, rather than a standard fixed dose.

2. What “pharmacokinetics” means (plain language)

Pharmacokinetics describes what the body does to a drug:

Absorption – how well the drug enters the bloodstream from the gut
Distribution – how effectively it reaches tissues such as the lungs
Metabolism – how quickly the liver breaks it down
Elimination – how the drug leaves the body

Differences at any of these stages explain why the same dose can be ineffective for one person and toxic for another.

3. Different generations of azole antifungals behave differently

Each generation of azole antifungal was designed to improve effectiveness, but chemical changes also altered how the body handles the drug.

First-generation azoles (older drugs)

Examples

Ketoconazole
Fluconazole (limited activity against Aspergillus)

Key features

Variable absorption
Shorter half-life
Less reliable lung penetration

Clinical relevance

Rarely used now for chronic aspergillosis

Second-generation azoles (mainstay treatment)

Examples

Itraconazole
Voriconazole
Posaconazole

Key features

Excellent lung and tissue penetration
Highly variable metabolism between people
Strong interaction with liver enzymes

Clinical relevance

Very effective
Blood levels vary widely
Dose adjustment and monitoring are often essential

Newer azoles

Example

Isavuconazole

Key features

More predictable absorption
Long, stable half-life
Fewer extreme peaks and troughs

Clinical relevance

Often better tolerated long-term
Monitoring still important, but dosing may be more stable

4. Why the “right dose” matters so much

Too little antifungal

Infection not adequately controlled
Symptoms persist or worsen
Risk of antifungal resistance
Fewer future treatment options

Too much antifungal

Liver irritation or damage
Nausea, appetite loss
Neurological or visual side effects
Drug accumulation, especially with long-term use

The aim is always the lowest dose that effectively controls the fungus.

https://ars.els-cdn.com/content/image/3-s2.0-B9780123868824000189-f18-07-9780123868824.jpg

5. How clinicians know whether the dose is right

No single test determines this. The correct dose is identified when three elements align:

1️⃣ Blood level testing (therapeutic drug monitoring)

Measures how much drug is actually in the bloodstream
Helps identify:
- Under-dosing
- Target-range dosing
- Toxic levels

2️⃣ Clinical response

Symptoms stabilise or improve
Fewer flare-ups or complications
Better day-to-day function

3️⃣ Safety monitoring

Liver and kidney blood tests
Review of side effects
Ongoing assessment of drug interactions

Only when effectiveness and safety are both acceptable is the dose considered “right”.

6. Why the right dose can change over time

A dose that was correct initially may later need adjustment because of:

Weight or body-composition changes
Age-related metabolic changes
New medications (including antibiotics or steroids)
Changes in liver or kidney function
Gradual drug accumulation during long-term therapy

Regular review is therefore expected and appropriate.

7. Is it sometimes impossible to find a stable dose?

Yes. For a minority of patients, a perfectly balanced dose cannot be found.

Reasons include:

Extremely fast or slow drug metabolism
A very narrow safety window
Long-term toxicity despite “acceptable” blood levels
Unavoidable interacting medications
Liver, kidney, or neurological vulnerability
Partial or full antifungal resistance

In these cases, the dose that controls the fungus and the dose that causes side effects may overlap.

This reflects biological limits, not treatment failure.

8. What clinicians do when a stable dose cannot be achieved

Options may include:

Switching to a different azole with different pharmacokinetics
Using modified dosing schedules (split dosing, slower titration)
Accepting a lower suppressive dose rather than full eradication
Considering non-azole antifungals where appropriate
Prioritising symptom control and quality of life

All are intentional, safety-focused decisions.

9. The central role of the specialist pharmacist

Specialist pharmacists are key to safe antifungal care, particularly for long-term azole therapy.

They play a critical role in:

Interpreting drug levels

Assessing whether a level is truly low or high
Accounting for dose timing and formulation
Preventing unnecessary or unsafe dose changes

Managing drug–drug interactions

Azoles interact with many common medicines, including:

Steroids and inhalers
Heart rhythm drugs
Blood thinners
Anti-epileptics
Pain medications

The specialist pharmacist:

Reviews the full medication list
Anticipates interactions before harm occurs
Advises on adjusting both interacting drugs

Individualising dosing

When standard doses do not work, they help design:

Non-standard doses
Split dosing schedules
Slow titration plans
Alternative azoles with different pharmacokinetics

Protecting patients during long-term treatment

They monitor:

Trends in liver and kidney tests
Signs of cumulative toxicity
Whether symptoms may be drug-related rather than disease-related

Coordinating care

They act as a bridge between:

Laboratory results
Clinical decision-making
Patient experience

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Their involvement often changes management, not just fine-tunes it.

10. Where antifungal drug level testing is done in the UK

In the UK, antifungal drug level testing is centralised.

Blood samples are taken locally
Samples are sent to specialist reference laboratories, most commonly the
Mycology Reference Centre Manchester
Results are returned to the local clinical team for interpretation

Patients managed through specialist services such as the
National Aspergillosis Centre
benefit from integrated expertise in antifungal pharmacology, imaging, and long-term monitoring.

This process is routine and standard for antifungal care.

11. Key reassurance for patients

Dose changes are normal and expected
Side effects are often biology-driven, not your fault
Blood tests make treatment safer, not riskier
Switching drugs is a planned strategy, not giving up

12. One-paragraph summary

Antifungal medicines—particularly azole antifungals—have complex and highly variable behaviour in the body, with a narrow balance between effectiveness and toxicity. Safe use requires individualised dosing, therapeutic drug monitoring, symptom review, and long-term safety checks. Specialist pharmacists play a central role in interpreting drug levels, managing interactions, and tailoring treatment. For some patients, a perfectly balanced dose cannot be achieved, and alternative strategies are required. This reflects biological complexity, not failure, and the overarching aim is always effective fungal control with the best possible long-term safety and quality of life.

by GAtherton

Airways mucus and aspergillosis

A clear, patient-friendly explainer

People living with aspergillosis often say that mucus is one of the hardest symptoms to manage — thick sputum, coughing fits, plugs that feel “stuck”, and flare-ups that seem to come out of nowhere. This explainer brings everything together in one place: what mucus is for, why aspergillosis causes so much of it, why it becomes abnormal, and what current and future treatments aim to do.

1. What is airway mucus and why do we need it?

Mucus is normal, healthy, and essential. Everyone produces it all the time.

Its main roles are to:

Trap inhaled particles (dust, spores, bacteria, pollution)
Protect the airway lining from drying and irritation
Support the immune system
Clear the lungs, using tiny moving hairs (cilia) that sweep mucus upwards so it can be swallowed or coughed out
(this clearance system is called the mucociliary escalator)

In healthy lungs:

Mucus is thin
Produced in small amounts
Cleared without you noticing it

2. Why aspergillosis causes excessive mucus

In aspergillosis, the lungs are under ongoing stress. Several factors combine:

Persistent immune activation

The immune system keeps reacting to Aspergillus material in the airways. Even when the fungus is controlled, inflammation can persist.

Allergic-type inflammation (especially in ABPA)

Allergic immune responses strongly stimulate mucus-producing cells, leading to:

Large volumes of mucus
Very sticky or rubbery sputum

Airway damage

Conditions commonly associated with aspergillosis (such as bronchiectasis or long-standing asthma) cause:

Widened or damaged airways
Poor mucus clearance
Pools of mucus that are hard to shift

Slowed clearance

Inflammation and infection impair cilia, so mucus:

Moves more slowly
Sits in the lungs longer
Becomes thicker and harder to clear

➡️ What starts as a protective response becomes a self-perpetuating problem.

3. Why thick mucus causes symptoms

Excess or abnormal mucus can:

Block airways → breathlessness and wheeze
Trigger coughing → especially overnight or on waking
Trap infection → repeated flare-ups
Reduce oxygen exchange
Increase fatigue and chest discomfort

Many patients describe it as:

“Glue-like”, “stringy”, “rubbery”, or “impossible to move”

4. Mucus plugs and crystals – why some mucus is so hard to clear

Mucus plugs

When mucus becomes very thick, it can:

Form plugs that partially or completely block airways
Show up on CT scans
Worsen breathlessness suddenly

Charcot–Leyden crystals

In allergic and eosinophilic airway disease (including allergic bronchopulmonary aspergillosis):

Breakdown products of allergic immune cells can form microscopic crystals
These crystals make mucus:
- Stiffer
- More irritating
- Harder to clear

Their presence is a sign of ongoing allergic inflammation, not infection alone.

5. Why managing mucus really matters

Mucus is not just an inconvenience. Poor mucus control can:

Increase infection risk
Drive repeated exacerbations
Worsen lung damage over time
Reduce quality of life and sleep
Increase hospital admissions

For aspergillosis, mucus management is core treatment, not optional.

6. What helps now (current approaches)

A. Thin the mucus

Good hydration
Nebulised saline (normal or hypertonic)
Selected mucolytic medicines (used carefully)

B. Move it out

Regular airway clearance physiotherapy
Breathing techniques (e.g. active cycle breathing)
Oscillating devices (flutter, Acapella, Aerobika)
Gentle, regular physical activity where possible

C. Reduce inflammation

Inhaled corticosteroids (when appropriate)
Oral steroids (used cautiously)
Biologic therapies for selected allergic or eosinophilic disease
Antifungal treatment when fungal burden is contributing

D. Treat infections early

Bacterial infections thicken mucus further
Prompt treatment reduces long-term damage

7. What research is doing differently (emerging therapies)

Research is moving beyond simply “loosening mucus”.

1. Reducing mucus production at source

Scientists are developing drugs that aim to:

Switch off excessive mucus secretion
Preserve normal protective mucus

This targets the mucus-producing cells directly.

2. Blocking the signals that drive over-production

Inflammation sends chemical signals telling airways to make more mucus. New treatments aim to:

Calm allergic and immune pathways
Prevent expansion of mucus-producing cells

Some current biologic therapies already reduce mucus indirectly; future drugs will be more precise.

3. Changing mucus structure

Instead of thinning everything, researchers are studying ways to:

Loosen the internal “mesh” of mucus
Prevent dense plugs from forming
Restore normal movement by cilia

4. Targeting mucus crystals

In allergic aspergillosis, research is exploring how to:

Reduce crystal formation
Calm the specific immune responses that create them

5. New inhaled and physical approaches

Early trials are testing:

Inhaled therapies designed to mobilise secretions
Treatments that improve airflow behind mucus plugs

6. Precision medicine

Future mucus treatments are likely to be:

Personalised
Based on inflammation type, fungal involvement, airway damage, and immune markers

Two people with aspergillosis may have very different mucus drivers — and need different solutions.

8. What this means for patients today

There is no single “anti-mucus cure” yet
Promising therapies are in research and early trials
Safety and long-term effects must be proven first

For now:

Regular airway clearance remains essential
Treating inflammation and infection promptly is crucial
Understanding why your mucus behaves as it does helps guide treatment

Key messages to remember

Mucus is normally protective
Aspergillosis turns a helpful system into a problem
Thick, sticky mucus reflects ongoing inflammation and airway damage
Crystals signal allergic involvement, not just infection
Research is moving toward preventing abnormal mucus formation, not just thinning it

by GAtherton

Hydrocortisone dosing in adrenal insufficiency

Why adrenal insufficiency can happen in people with aspergillosis

Many people with aspergillosis, particularly those with asthma-related conditions such as allergic bronchopulmonary aspergillosis (ABPA) or more severe chronic lung disease, need treatment with steroid medicines at some point. These treatments — often essential to control inflammation, protect the lungs, and improve breathing — may include repeated or long-term courses of steroids such as prednisolone.

When steroid treatment is used over time, it can reduce the body’s own production of cortisol by the adrenal glands. In some people, the adrenal glands do not fully recover, leading to adrenal insufficiency. Cortisol is a vital hormone that helps the body manage energy, illness, infection, and physical stress. When it cannot be made reliably, hydrocortisone replacement is needed to keep the body safe and functioning.

In this situation, hydrocortisone is prescribed to replace the cortisol your body can no longer make, usually after prednisolone has been reduced or stopped, or when prednisolone is no longer needed to control lung inflammation but adrenal support is still required.

Adrenal insufficiency in people with aspergillosis is not a failure and not something you have caused. It is a recognised consequence of necessary treatment for a serious, long-term condition. With the right information, a personalised dosing plan, and medical support, adrenal insufficiency can be managed safely alongside aspergillosis.

A patient guide to everyday (basal) dosing, higher-dose needs, and short-term stress dosing

If you take hydrocortisone because you have adrenal insufficiency, understanding how your dose works — both day to day and during illness or stress — is essential for your safety and wellbeing.

This guide explains:

What your basal (everyday) dose is for
Why some people need higher basal doses
When and how stress dosing is used — and why it is short term
Why some doctors may hesitate — and how to work safely with them
Where to find trusted patient and clinician resources

Very important first point ❗

Any changes to your hydrocortisone dose must be agreed in advance with a doctor or specialist nurse who knows your adrenal insufficiency.

This includes:

Your usual daily dose
Your stress-dosing (“sick day”) plan
Emergency injection instructions

This guide does not replace medical advice.
It is designed to help you understand your treatment and communicate clearly with healthcare professionals.

1) Your basal (everyday) hydrocortisone dose

What the basal dose is for

Your basal dose is the hydrocortisone you take on an ordinary day, when you are not ill or under unusual stress. Its purpose is to:

Replace the cortisol your body cannot make reliably
Support normal daily function (energy, blood pressure, mood)
Help your body feel stable and safe
Reduce the risk of chronic under-replacement

It is replacement, not treatment for inflammation.

A key point many patients are not told

Being consistently under-replaced does not help adrenal recovery.

Ongoing symptoms such as:

Constant exhaustion
Dizziness or nausea on standing
Brain fog or low mood
Poor tolerance of everyday stress
Frequent “crashes” or infections

can delay recovery, not speed it. Stability supports healing.

What doctors usually mean by a “physiological” dose

Most adults naturally produce the equivalent of about 15–25 mg of hydrocortisone per day.

Doctors aim for a dose in this range and adjust for:

Body size
Activity level
Other medical conditions
Individual response

This is replacement, not “high-dose steroids”.

How basal hydrocortisone is usually taken

To mimic the body’s natural rhythm, doses are often split:

A larger dose in the morning
Smaller doses later in the day
Avoiding late evening doses where possible

This supports:

Energy and blood pressure
Sleep
Mood and concentration

Signs your basal dose may be too low

Tell your doctor if you have persistent:

Severe fatigue despite rest
“Wired but empty” feeling
Dizziness, nausea, or salt craving
Poor concentration or memory
Low mood or anxiety
Frequent need for rescue or stress doses

These symptoms matter even if blood tests look reassuring.

Blood tests are only part of the picture

Cortisol and ACTH tests:

Help with diagnosis
Are less helpful for adjusting daily dose
Do not always reflect how well you function

Doctors experienced with adrenal insufficiency rely heavily on how you feel and cope day to day.

The right balance

Rather than “as low as possible,” a safer aim is:

Low enough to avoid overtreatment, but high enough to live a stable, functional life.

Living in constant deficit is not success.

2) When a higher basal dose may be appropriate

Some people with adrenal insufficiency — particularly those with chronic illness — may genuinely need a higher basal hydrocortisone dose (for example 25–30 mg/day).

This does not automatically mean overtreatment.

Well-recognised examples include:

Chronic inflammatory lung disease (including ABPA)

Ongoing airway inflammation and immune activation
Recurrent infective or inflammatory flares
The body may never be in a true “resting” state
Standard doses may leave patients under-replaced
A stable higher dose can reduce repeated stress dosing and improve daily function

Frequent infections or slow recovery

Repeated illness or prolonged recovery
Frequent “temporary” stress dosing just to cope with everyday life

Long-standing steroid-induced adrenal insufficiency

Years of prednisolone or similar treatment
Deep suppression of the adrenal system

Larger body size or higher metabolic demand

Cortisol needs vary with body size and activity

Autonomic symptoms or low blood pressure

Postural dizziness or faintness
Often benefit from a higher morning dose

Clinical clue:
If someone repeatedly needs stress dosing just to manage ordinary days, their basal dose may be too low for their current physiology.

Important reassurance

Higher basal doses can be appropriate, temporary, or longer-term
They do not automatically prevent recovery
Ongoing inflammation and repeated physiological stress suppress recovery more than adequate replacement
Doses should always be prescribed, documented, and reviewed

3) Stress dosing — when your body temporarily needs more

What stress dosing means

A healthy body automatically makes more cortisol during:

Illness or infection
Fever
Vomiting or diarrhoea
Injury or trauma
Severe pain
Surgery or medical procedures
Major physical stress

If you have adrenal insufficiency:
➡️ your body cannot do this, so doctors prescribe stress dosing in advance as part of your safety plan.

Stress dosing is essential — but it is short term

Stress dosing is meant to last only as long as the stress lasts.

It covers a temporary increase in need, not your everyday requirements.

What “short term” usually means

Stress dosing may last:

24–48 hours for minor illness or fever
Several days for infections or recovery from injury
During and immediately after surgery or procedures

Your doctor should advise:

When to increase
How much to increase
When and how to return to your usual dose

Why stress dosing should not continue indefinitely

If higher doses are needed for longer, something usually needs review:

Infection or inflammation has not settled
The basal dose may be too low
Another medical problem is present

If stress dosing is still needed after the original stress has passed, it’s time to talk to your doctor.

Stepping back down safely

Doctors usually advise returning to baseline
Sometimes a 1–2 day step-down is used
You should not remain on stress doses “just in case”

Stress dosing does NOT:

Stop adrenal recovery
Mean you are “failing”
Cause long-term harm when used correctly

Not stress dosing can:

Make you seriously unwell
Delay recovery
Lead to adrenal crisis

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https://www.endocrinology.org/media/3705/nhs-steroid-card-front.jpg?format=webp&quality=20&width=700

4) Why some doctors seem hesitant

Doctors outside endocrinology (GPs, A&E, ward teams):

Are trained to minimise steroid use
Often think of steroids only as anti-inflammatory drugs
May rarely manage adrenal insufficiency

What they may not realise immediately:

Your hydrocortisone is replacing a missing hormone — it is essential, not extra.

5) How to advocate safely (with medical backing)

It is appropriate to say:

“I have adrenal insufficiency. My doctor has advised stress dosing during illness to prevent adrenal crisis.”

If you have them, show:

Your Steroid Emergency Card
A written stress-dosing plan
A clinic letter or summary

6) Trusted resources & further support (with links)

The following organisations provide reliable, clinician-endorsed information on adrenal insufficiency, hydrocortisone replacement, stress dosing, and emergency care.
They are widely recognised by NHS endocrinology teams and safe to share with patients, families, and healthcare professionals.

UK patient and professional resources

Addison’s Disease Self-Help Group (ADSHG)
Website: https://www.addisonsdisease.org.uk

What it offers:

Clear explanations of basal vs stress dosing
Patient-friendly sick-day rules
Emergency hydrocortisone injection guidance
Downloadable patient leaflets used in NHS clinics
Webinars, helpline, and peer support

Why it’s useful:
ADSHG explicitly supports individualised dosing and crisis prevention.

Society for Endocrinology
Steroid Emergency Card & adrenal crisis guidance:
https://www.endocrinology.org/clinical-practice/steroid-emergency-card/

Why it’s useful:

Highly trusted by doctors, A&E, and ward teams
Clear professional wording that reassures non-specialists
Supports rapid decision-making in emergencies

NHS (England)
Steroid Emergency Card information:
https://www.nhs.uk/conditions/steroid-emergency-card/

Why it’s useful:

Official NHS backing
Useful for legitimacy in emergency or inpatient settings

International patient resources (useful supplements)

Endocrine Society
Patient information on adrenal insufficiency:
https://www.endocrine.org/patient-engagement/endocrine-library/adrenal-insufficiency

Why it’s useful:

Clear explanations of cortisol physiology
Conservative, authoritative tone
Helpful for patients seeking international consensus

National Adrenal Diseases Foundation (NADF)
Website: https://www.nadf.us

What it offers:

Practical sick-day rules
Emergency preparedness guidance
Injection training resources

Particularly helpful for patients with long-standing adrenal insufficiency or frequent illness.

Resources especially relevant for ABPA & chronic lung disease

National Aspergillosis Centre
Website: https://mft.nhs.uk/wythenshawe/services/infectious-diseases/national-aspergillosis-centre/

Why it’s relevant:

Specialist centre where ABPA and adrenal insufficiency often overlap
Supports personalised care plans in complex disease

Aspergillosis Trust
Website: https://www.aspergillosistrust.org

Why it’s useful:

Patient-focused education and advocacy
Helps explain the chronic physiological stress of ABPA
Supports conversations about higher basal hydrocortisone needs

Quick-access patient checklist (phone / wallet)

Patients are encouraged to keep:

Steroid Emergency Card
Sick-day rules (ADSHG)
Personal stress-dosing plan (agreed with doctor)
Clinic letter or summary

Many patients keep photos of these documents on their phone for emergencies.

Final reassurance

These resources support — not replace — medical advice.
They exist to help patients stay safe, informed, and confident when managing hydrocortisone and communicating with healthcare professionals.

by GAtherton

Muscle Cramps in Aspergillosis (Including ABPA and CPA): Causes, Triggers, and What May Help

Key Points

Contents

Overview

Why do muscle cramps happen?

How is this linked to aspergillosis and its treatment?

Additional considerations in chronic pulmonary aspergillosis (CPA)

Common Contributing Factors

What May Help Reduce Cramps

When to Seek Medical Advice

Common Questions

Are muscle cramps a symptom of aspergillosis?

Why do cramps happen at night?

If I take magnesium, shouldn’t cramps stop?

Are cramps more important to report in CPA?

References & Further Reading

Author & Review Information

Why Headaches Can Occur in Aspergillosis

Key Points

Table of Contents

Overview

Sinus involvement (common cause)

Inflammation and immune response

Allergic-type responses (e.g. ABPA)

Medication effects

Sleep disturbance and night symptoms

Breathing and oxygen levels

General health factors

Understanding headache patterns

Headaches in Aspergillosis: Interactive Decision Aid

1. Where is the pain mainly felt?

2. When is it most noticeable?

3. What does it feel like?

4. What other features are present?

5. Are there any red flags?

Possible contributors

Common questions

Are headaches a recognised symptom of aspergillosis?

Can antifungal treatment improve headaches?

Are “histamine-type” headaches part of aspergillosis?

Why do my headaches change over time?

When to seek medical advice

Summary

Author and review

References

How Inflammation in One Part of the Body Can Affect the Rest of the Body

Key points

Table of contents

What is inflammation?

Why inflammation does not always stay local

How the body communicates during inflammation

1. Chemical messengers in the blood

2. Organ-to-organ immune cross-talk

3. Nerve signalling between the body and brain

4. Stress, hormones, and metabolism

Common whole-body effects of inflammation

Fatigue

Brain fog and mood changes

Heart and blood vessel effects

Kidney effects

Muscle weakness and reduced stamina

Why this matters in lung disease and aspergillosis

Acute inflammation versus chronic inflammation

Acute inflammation

Chronic inflammation

What can help?

When to seek medical advice

Common questions

Does inflammation always damage the whole body?

Can one inflamed organ affect another?

Can inflammation cause fatigue even if blood tests are not dramatically abnormal?

Is this relevant to chronic lung disease?

References

Managing fatigue and energy in aspergillosis and allergic fungal lung disease

Key points

Contents

Why people with lung disease feel exhausted after exertion

What is happening in the lungs and body?

Inflamed airways

Mucus affecting airflow