Medical illustration showing Aspergillus otomycosis, a fungal infection of the external ear canal, including fungal debris, symptoms, diagnosis and treatment principles.

Aspergillus Otomycosis: A 2026 Update for Clinicians and Expert Patients

Medical illustration showing Aspergillus otomycosis, a fungal infection of the external ear canal, including fungal debris, symptoms, diagnosis and treatment principles.
Illustration of Aspergillus otomycosis showing fungal infection within the external ear canal, common symptoms, diagnosis and treatment approaches.

Article type: Clinical and expert-patient evidence updateIntended audience: Ear, nose and throat clinicians, infectious diseases specialists, medical mycologists, general practitioners, specialist nurses, expert patients and carers.Last reviewed: June 2026

Key points

  • Otomycosis is a fungal infection of the external auditory canal. It is often described as fungal otitis externa.
  • Aspergillus species and Candida species are the most commonly reported causes.
  • Older reports often describe Aspergillus niger as the main cause, but molecular methods show that related black Aspergillus species, including Aspergillus tubingensis, may previously have been misidentified as A. niger.
  • Diagnosis is usually clinical, supported where possible by microscopy, fungal culture and species identification.
  • Successful treatment usually requires careful cleaning of the ear canal as well as appropriate topical antifungal treatment.
  • Before topical treatment is used, clinicians should assess whether the tympanic membrane is intact, because some preparations may be unsafe if there is perforation, grommets, a mastoid cavity or previous ear surgery.
  • Most cases are superficial, but recurrent, severe or treatment-resistant disease should prompt reassessment for mixed bacterial infection, diabetes, immunosuppression, hearing aid moulds, foreign body, chronic ear disease or extension beyond the external canal.
  • Invasive or necrotising external otitis is rare but serious and requires urgent specialist assessment.
  • Sudden hearing loss, facial weakness, severe persistent pain, mastoid swelling or tenderness, neurological symptoms, or infection in a person with diabetes or significant immunosuppression should be treated as red flags.

Contents

What is otomycosis?

Otomycosis is a fungal infection of the external auditory canal, the skin-lined passage leading from the outer ear to the eardrum. It is also called fungal otitis externa. The infection may be acute, subacute or chronic, and it can be mistaken for bacterial otitis externa, eczema, wax, chronic discharge or non-specific inflammation.

In most people, otomycosis is a superficial infection of the outer ear canal. It can be uncomfortable, persistent and prone to recurrence, but it is usually treatable when the ear is examined, cleaned and treated appropriately. Rarely, particularly in people with diabetes, immunosuppression, previous ear surgery or severe persistent symptoms, infection may spread beyond the ear canal and become invasive.

Plain-English summary: most Aspergillus ear infections affect the outer ear canal. They are usually not the same as invasive aspergillosis in the lungs or bloodstream, but they can still need specialist ear care to clear the infection safely.

Aspergillus ear infection is different from lung aspergillosis

Many people searching online for Aspergillus find information about chronic pulmonary aspergillosis, allergic bronchopulmonary aspergillosis or invasive aspergillosis. These are different conditions.

Aspergillus otomycosis usually affects the external ear canal only. It is usually a local fungal infection rather than a whole-body infection. It does not usually mean that a person has invasive aspergillosis, chronic pulmonary aspergillosis or allergic bronchopulmonary aspergillosis.

However, people with existing lung disease, diabetes, immune suppression or complex medical histories should still tell their clinician about these conditions, because they may affect assessment and treatment decisions.

Why Aspergillus matters

Aspergillus is a common environmental mould. Its spores are present in air, dust, soil, compost, decaying vegetation and indoor environments. In the ear canal, fungal growth is favoured when local conditions change. Moisture, trauma to the skin, loss of normal wax protection, altered acidity, previous antibiotic or steroid drops, retained debris and obstruction from hearing aid moulds or ear plugs can all make fungal overgrowth more likely.

In otomycosis, Aspergillus species are among the most frequently reported fungi. They are particularly important because their appearance in the ear can be striking, with black, grey, greenish, yellow-white or fluffy debris. However, appearance alone is not enough for precise species identification.

Epidemiology and why cases may be missed

Reported prevalence varies considerably between studies and geographical regions. Otomycosis is more common in some warm, humid or dusty environments, but it is reported worldwide, including in the United Kingdom. In UK practice, it may be considered particularly in chronic, recurrent or treatment-resistant otitis externa.

Cases may be missed because symptoms overlap with bacterial otitis externa and inflammatory ear conditions. A patient may be treated repeatedly with antibacterial or steroid-containing ear drops before fungal infection is considered. In some cases, antibacterial treatment may suppress bacteria while allowing fungi to overgrow.

A 2025 systematic review highlighted increasing use of molecular methods for species identification, although many published studies still rely primarily on microscopy and culture.

Causative Aspergillus species

Older articles often refer to Aspergillus niger as the dominant Aspergillus species in otomycosis. This remains a useful clinical shorthand, but it is no longer the whole story. Modern molecular identification has shown that black Aspergillus isolates are a complex group and may include species such as Aspergillus tubingensis and other members of the Aspergillus niger complex.

Reported Aspergillus species in otomycosis and fungal otitis externa include:

  • Aspergillus niger complex, including related black Aspergillus species
  • Aspergillus tubingensis
  • Aspergillus flavus
  • Aspergillus fumigatus
  • Aspergillus terreus complex, reported occasionally in superficial infection series but apparently less common than the Aspergillus niger complex or Aspergillus flavus

Clinical relevance: species-level identification is not always needed for straightforward cases that respond to topical treatment. It becomes more important in recurrent, invasive, immunocompromised or treatment-resistant infection, or where systemic antifungal treatment is being considered.

Risk factors

Otomycosis usually develops when the normal protective environment of the ear canal is disrupted. Important risk factors include:

  • warm, humid or dusty environments
  • frequent swimming or repeated water exposure
  • use of cotton buds, ear picking or other trauma to the ear canal
  • previous or repeated antibacterial ear drops
  • topical steroid use in the ear
  • hearing aids, ear plugs or occlusive moulds
  • excess wax, retained debris or foreign material
  • chronic otitis externa or chronic otitis media
  • previous ear surgery or mastoid cavity
  • tympanic membrane perforation
  • diabetes, especially if poorly controlled
  • immunosuppression, including chemotherapy, transplant medicines, prolonged high-dose corticosteroids and some biological therapies
  • skin conditions affecting the ear canal, such as eczema or seborrhoeic dermatitis

Plain-English summary: fungi grow more easily when the ear canal is damp, damaged, blocked, repeatedly treated with antibiotics, or when a person’s immune defences are reduced.

Symptoms and clinical features

Symptoms vary. Some patients have mild itching and fullness, while others have marked discomfort, discharge or hearing loss. Common symptoms include:

  • itching in the ear
  • ear fullness or blockage
  • discharge from the ear
  • reduced hearing, often due to debris blocking the canal
  • ear discomfort or pain
  • tinnitus or ringing in the ear
  • scaling, inflammation or visible debris in the ear canal

Severe pain, persistent night pain, swelling around the ear, tenderness or swelling over the mastoid bone behind the ear, fever, persistent or severe dizziness, facial weakness, severe headache, cranial nerve symptoms or symptoms in a person with diabetes or immunosuppression should raise concern for more serious disease.

Sudden hearing loss should be treated as a medical emergency and assessed urgently, regardless of whether otomycosis is suspected.

Diagnosis

Clinical examination

Diagnosis is often suspected by otoscopic or microscopic examination of the ear canal. Typical findings may include fungal debris, spores, hyphae, wet or dry masses, inflammation, scaling, discharge and obstruction. Black, grey, white, yellow-green or fluffy material may be seen, but visual appearance does not reliably identify the species.

Assessment should include:

  • extent of external canal inflammation
  • presence of fungal debris or discharge
  • degree of canal obstruction
  • condition of the tympanic membrane
  • evidence of perforation, grommets, mastoid cavity or prior surgery
  • features suggesting bacterial co-infection
  • signs of spread beyond the external canal

Microscopy and fungal culture

Microscopy can demonstrate fungal hyphae or yeast forms. Culture can identify whether Aspergillus, Candida or another fungus is present. Bacterial culture may also be useful if mixed infection is suspected.

Culture is especially helpful when disease is recurrent, severe, atypical, invasive, not responding to standard treatment, or occurring in a person with diabetes, immunosuppression or previous ear surgery.

Molecular identification

Molecular methods can identify Aspergillus species more accurately than morphology alone. This matters because older culture-based reports may have grouped several black Aspergillus species under Aspergillus niger. Molecular identification may also help in epidemiological studies and difficult clinical cases.

For routine mild otomycosis, molecular identification is not always necessary. For persistent, recurrent or invasive disease, species-level identification and antifungal susceptibility testing may help guide treatment.

Antifungal susceptibility testing

Antifungal susceptibility testing is not required for every simple case. It should be considered when there is treatment failure, recurrent disease, unusual species, invasive infection or planned systemic antifungal therapy. Susceptibility patterns may vary between Aspergillus species, although resistance testing is not routinely required for uncomplicated superficial disease.

When to consider imaging

Imaging is not needed for uncomplicated superficial otomycosis. It may be required if there is concern about necrotising external otitis, skull base osteomyelitis, mastoid involvement, middle ear extension, cranial nerve involvement or deep tissue spread. Imaging decisions should be made by ear, nose and throat, infectious diseases, radiology and microbiology or mycology specialists as appropriate.

Differential diagnosis

Conditions that can resemble Aspergillus otomycosis include:

  • bacterial otitis externa
  • chronic otitis externa
  • eczema or dermatitis of the ear canal
  • impacted wax
  • foreign body
  • chronic suppurative otitis media
  • cholesteatoma
  • otitis media with perforation
  • necrotising external otitis
  • malignancy of the external canal or temporal bone, rarely

Failure to respond to usual antibacterial treatment should prompt reconsideration of the diagnosis rather than repeated courses of the same treatment.

Treatment principles

Treatment depends on severity, tympanic membrane status, immune status, recurrence, species where known, and whether infection is limited to the outer ear canal. Local ear, nose and throat practice and local antimicrobial guidance should be followed.

1. Aural toilet and debridement

Careful cleaning of the ear canal is central to management. Fungal debris can block the canal, protect organisms from topical treatment and contribute to hearing loss. Aural toilet, often using microsuction or careful debridement, is usually best performed by a trained clinician using appropriate equipment, especially if the canal is swollen, painful, obstructed, or if the tympanic membrane cannot be seen.

Patients should not attempt deep cleaning with cotton buds, hair grips, ear candles or improvised tools. These can damage the ear canal, push debris deeper, worsen inflammation or perforate the eardrum.

Ear irrigation is not usually the preferred approach for suspected otomycosis, because retained moisture may encourage fungal growth and because irrigation may be unsafe if there is tympanic membrane perforation, grommets or previous ear surgery.

2. Topical antifungal treatment

Most uncomplicated otomycosis is treated with topical antifungal therapy after cleaning. Reported agents include clotrimazole, miconazole, nystatin, ciclopirox and other locally used preparations. Different countries and ear, nose and throat services use different formulations, and the evidence does not clearly establish one universally superior topical agent for all cases.

Choice of topical treatment should consider:

  • likely organism: mould versus yeast
  • whether the tympanic membrane is intact
  • previous ear surgery, mastoid cavity or grommets
  • local formulary and ear, nose and throat practice
  • potential ototoxicity
  • patient tolerance and adherence
  • whether the canal needs repeat cleaning

3. Tympanic membrane safety

Assessment of the eardrum is important. Some topical agents, antiseptics, acidic preparations or combination drops may be unsafe if the tympanic membrane is perforated or if there are grommets, a mastoid cavity or previous ear surgery. If the eardrum cannot be visualised, treatment should be chosen cautiously and specialist ear, nose and throat advice may be needed.

Important safety point

Patients should not put unprescribed antifungal, antiseptic, acidic, oil-based or herbal preparations into the ear. This is especially important if there is discharge, severe pain, previous ear surgery, grommets, suspected perforated eardrum, sudden hearing loss, dizziness or facial weakness.

4. Mixed bacterial and fungal infection

Mixed infection can occur. If bacterial infection is suspected, bacterial culture and targeted antibacterial treatment may be needed. However, repeated broad-spectrum antibacterial drops without reassessment may encourage fungal overgrowth and delay recognition of otomycosis.

5. Hearing aids, earmoulds and ear plugs

Hearing aids, earmoulds and ear plugs can trap moisture and debris in the ear canal. They may also act as a continuing source of irritation or contamination if not cleaned properly. In recurrent otomycosis, hearing aids and moulds should be reviewed, cleaned according to manufacturer guidance and, where appropriate, assessed by audiology or ear, nose and throat services.

6. Diabetes and immune suppression

People with diabetes or significant immune suppression need particular care, because severe or invasive external ear infection is more likely in these groups. Optimising glycaemic control may help reduce the risk of severe or recurrent infection. Clinicians should consider whether persistent or severe otitis externa in a person with diabetes could represent necrotising external otitis.

7. Systemic antifungal treatment

Systemic antifungal treatment is not usually required for uncomplicated superficial otomycosis. It may be considered in selected situations, including:

  • invasive or necrotising external otitis
  • extension into the middle ear, mastoid, skull base or surrounding tissues
  • severe infection in an immunocompromised patient
  • persistent disease where topical therapy is not possible, unsafe or ineffective
  • cases requiring multidisciplinary ear, nose and throat, infectious diseases and mycology input

Systemic antifungal choice should be guided by species identification, susceptibility testing, site and extent of infection, drug interactions, renal and liver function, and local specialist advice. Azole antifungals such as itraconazole, voriconazole, posaconazole and isavuconazole have important drug interactions and monitoring requirements.

Recurrent or treatment-resistant otomycosis

Recurrent otomycosis is common in some series. Recurrence does not always mean that the original treatment was wrong; it may reflect ongoing risk factors or incomplete clearance of debris.

When otomycosis recurs or fails to respond, clinicians should reassess:

  • Was the ear canal adequately cleaned?
  • Can the tympanic membrane be seen?
  • Is there perforation, chronic otitis media or mastoid cavity disease?
  • Is there a hearing aid mould, ear plug or foreign body contributing?
  • Is the patient using cotton buds or self-cleaning the ear?
  • Is there persistent water exposure?
  • Is there eczema, dermatitis or another inflammatory ear condition?
  • Is there mixed bacterial and fungal infection?
  • Has microscopy or culture confirmed the organism?
  • Is species-level identification or susceptibility testing needed?
  • Is the patient diabetic or immunocompromised?
  • Is there severe pain, mastoid tenderness or evidence of deeper spread?

Invasive Aspergillus ear infection and necrotising external otitis

Most Aspergillus otomycosis is superficial. However, fungal infection of the external ear can rarely become invasive, particularly in people with diabetes, immunosuppression, severe chronic ear disease or previous ear surgery.

Necrotising external otitis, historically called malignant external otitis, is a severe infection that may involve soft tissues, cartilage, temporal bone or skull base. It is most often bacterial, especially due to Pseudomonas aeruginosa, but fungal cases including Aspergillus and Candida are reported. Fungal necrotising external otitis can be difficult to diagnose and may require prolonged treatment.

Features that should raise concern include:

  • severe, persistent or worsening ear pain, especially at night
  • pain out of proportion to examination findings
  • persistent discharge despite appropriate treatment
  • granulation tissue in the ear canal
  • facial weakness or other cranial nerve symptoms
  • persistent, severe or worsening dizziness, particularly with severe pain, hearing loss or neurological symptoms
  • severe headache or neurological symptoms
  • swelling, redness or cellulitis around the ear
  • tenderness, swelling or redness over the mastoid bone behind the ear
  • diabetes, especially if poorly controlled
  • immunosuppression
  • evidence of mastoid, middle ear or skull base involvement

Suspected invasive or necrotising disease needs urgent ear, nose and throat assessment, microbiological sampling, imaging and specialist antimicrobial or antifungal planning. This is not a condition for self-treatment.

Practical advice for patients and expert patients

Patients can support recovery by protecting the ear canal while treatment is underway. Advice should be individualised by the treating clinician, but common measures include:

  • keep the affected ear dry unless advised otherwise
  • avoid swimming until cleared by a clinician
  • do not use cotton buds or insert objects into the ear
  • use prescribed drops exactly as directed
  • attend follow-up if symptoms persist, because repeat cleaning may be needed
  • tell the clinician about diabetes, immune problems, steroid use, biological therapies, chemotherapy, transplant medicines or previous ear surgery
  • ask whether hearing aids, earmoulds or ear plugs need cleaning or review
  • report severe pain, dizziness, facial weakness, worsening hearing loss or persistent discharge urgently

Important: online images of invasive aspergillosis can be frightening and often do not represent ordinary otomycosis. Most Aspergillus ear infections are local infections of the outer ear canal. The key is proper assessment, safe cleaning and appropriate treatment.

Frequently asked questions

Is Aspergillus otomycosis rare?

It depends on the setting. Otomycosis is common in some warm and humid regions but is less commonly recognised in many UK clinics. Aspergillus otomycosis may be unfamiliar to clinicians who do not often see fungal ear disease.

Is it the same as invasive aspergillosis?

Usually, no. Most Aspergillus otomycosis is a superficial infection of the outer ear canal. Invasive disease is rare but important, especially in people with diabetes, immunosuppression, severe pain or persistent infection.

Can an ear infection cause symptoms elsewhere in the body?

Otomycosis itself would not usually cause breathlessness, chest symptoms or systemic illness. If a person with suspected otomycosis is also breathless, has chest pain, fever, low oxygen levels or feels very unwell, those symptoms should be assessed separately and promptly.

Can it affect hearing?

Yes. Hearing may be reduced if the ear canal is blocked by fungal debris, discharge or swelling. Hearing often improves when the canal is cleaned and inflammation settles. Sudden hearing loss should be treated as a medical emergency and assessed urgently.

Should every case be cultured?

Not necessarily. Straightforward cases may be treated clinically. Culture and microscopy are more useful when symptoms are recurrent, severe, atypical, treatment-resistant, associated with perforation or surgery, or occur in an immunocompromised patient.

Are antifungal ear drops enough?

Often, topical treatment is effective, but drops may not work well if the ear canal is blocked with debris. Cleaning the canal is often as important as the antifungal medicine itself.

Can patients buy something and treat it themselves?

This is not recommended. Ear symptoms can have several causes, and some substances may be unsafe if the eardrum is perforated. Patients should seek clinical assessment before putting unprescribed antifungal, antiseptic, acidic, herbal or oil-based preparations into the ear.

Why does otomycosis come back?

Recurrence can happen if the canal remains damp, debris persists, the ear is repeatedly traumatised, a hearing aid mould traps moisture, eczema is present, antibiotics are repeatedly used, or an underlying condition such as diabetes or immune suppression is not recognised.

When to seek urgent medical help

Patients should seek urgent medical advice if they have:

  • severe or worsening ear pain
  • pain that wakes them at night
  • swelling, redness or tenderness around the ear
  • tenderness, swelling or redness over the mastoid bone behind the ear
  • persistent discharge despite treatment
  • sudden hearing loss or rapidly worsening hearing
  • persistent, severe or worsening dizziness
  • severe headache or vomiting
  • facial weakness or changes in facial movement
  • confusion, fever or feeling very unwell
  • diabetes, immune suppression or recent chemotherapy or transplant treatment with ear infection symptoms
  • previous ear surgery, grommets or known eardrum perforation with new discharge or pain

These symptoms do not prove invasive infection, but they should be assessed promptly.

Evidence gaps and uncertainty

The evidence base for otomycosis is improving but remains limited. Many studies are single-centre observational series from regions where otomycosis is more common. Treatment studies vary in diagnostic criteria, topical agents, follow-up duration and whether cleaning was standardised. There is no single universally accepted treatment regimen for all cases.

Important gaps include:

  • limited high-quality randomised trials comparing topical antifungal treatments
  • variable reporting of tympanic membrane status and previous ear surgery
  • inconsistent use of fungal culture, molecular identification and susceptibility testing
  • limited data on recurrence prevention
  • limited evidence specific to UK practice
  • uncertainty about the best systemic antifungal approach in rare invasive cases

For these reasons, this article should support but not replace specialist clinical judgement.

References

  1. Nazari T, Peymaeei F, Ghazi Mirsaid R, et al. Otomycosis: a systematic review and meta-analysis of prevalence and causative agents in the era of molecular diagnostics. BMC Infectious Diseases. 2025;25(1). doi: 10.1186/s12879-025-10954-y. PubMed
  2. Bojanović M, Stalević M, Arsić-Arsenijević V, et al. Etiology, Predisposing Factors, Clinical Features and Diagnostic Procedure of Otomycosis: A Literature Review. Journal of Fungi. 2023;9(6):662. doi: 10.3390/jof9060662. PubMed
  3. Wiegand S, Berner R, Schneider A, Lundershausen E, Dietz A. Otitis Externa: Investigation and Evidence-Based Treatment. Deutsches Ärzteblatt International. 2019. doi: 10.3238/arztebl.2019.0224. PubMed
  4. Koltsidopoulos P, Skoulakis C. Otomycosis With Tympanic Membrane Perforation: A Review of the Literature. Ear, Nose & Throat Journal. 2019;99(8):518–521. doi: 10.1177/0145561319851499. PubMed
  5. Mtibaa L, Halwani C, El Hamdi M, et al. A retrospective study of 43 cases of fungal malignant external otitis. Pan African Medical Journal. 2022;41. doi: 10.11604/pamj.2022.41.287.29585. PubMed
  6. Szigeti G, Sedaghati E, Mahmoudabadi AZ, et al. Species assignment and antifungal susceptibilities of black aspergilli recovered from otomycosis cases in Iran. Mycoses. 2011;55(4):333–338. doi: 10.1111/j.1439-0507.2011.02103.x. PubMed
  7. Jimenez-Garcia L, Celis-Aguilar E, Díaz-Pavón G, et al. Efficacy of topical clotrimazole vs. topical tolnaftate in the treatment of otomycosis: a randomized controlled clinical trial. Brazilian Journal of Otorhinolaryngology. 2020;86(3):300–307. doi: 10.1016/j.bjorl.2018.12.007. PubMed
  8. Mofatteh MR, Naseripour Yazdi Z, Yousefi M, et al. Comparison of the recovery rate of otomycosis using betadine and clotrimazole topical treatment. Brazilian Journal of Otorhinolaryngology. 2018;84(4):404–409. doi: 10.1016/j.bjorl.2017.04.004. PubMed
  9. Mao C, Li A, Hu J, et al. Efficient and accurate diagnosis of otomycosis using an ensemble deep-learning model. Frontiers in Molecular Biosciences. 2022;9:951432. doi: 10.3389/fmolb.2022.951432. PubMed
  10. Feng Y, Zhang Z, Fang W, et al. Profiling Drug Susceptibility and Species Identification of Aspergillus Isolates From Patients With Superficial Infection. Mycoses. 2025;68(4). doi: 10.1111/myc.70059. PubMed
  11. NICE Clinical Knowledge Summaries. Otitis externa. NICE CKS

Author and review information

Article type: Clinical and expert-patient evidence update

Intended audience: Ear, nose and throat clinicians, infectious diseases specialists, medical mycologists, general practitioners, specialist nurses, patients and carers seeking detailed information.

Last reviewed: June 2026

Review note: This article is for information and education. It should not replace assessment by a qualified clinician. Treatment choices depend on examination findings, tympanic membrane status, culture results where available, medical history, immune status and local prescribing guidance.

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by GAtherton

Patient with Allergic Bronchopulmonary Aspergillosis (ABPA) considering biologic treatment, alongside an infographic explaining why steroids and antifungal medicines are often used before biologics.

Why Do People With ABPA Usually Have to Try Steroids and Antifungals Before Biologics?

Last reviewed: June 2026

Key points

  • Many people with Allergic Bronchopulmonary Aspergillosis (ABPA) report significant improvements after starting biologic medicines.
  • Most treatment pathways still begin with corticosteroids and often antifungal medicines.
  • Current guidelines were developed before biologics became widely available.
  • Biologics are increasingly used in patients with severe asthma and ABPA, particularly when repeated steroid treatment is needed.
  • Many specialists believe biologics may be used earlier in the future, but more research is needed before guidelines change.

Quick answer

People with Allergic Bronchopulmonary Aspergillosis (ABPA) are usually treated first with corticosteroids and often antifungal medicines because these treatments form the basis of current clinical guidelines and can work quickly during flare-ups. Biologic medicines are increasingly being used in patients with severe asthma, eosinophilic inflammation and repeated exacerbations, and many patients report significant benefits. Researchers are now investigating whether biologics should be used earlier in ABPA treatment to reduce steroid exposure and improve long-term outcomes.

Why this question matters

One of the most common questions asked in patient support groups is: “If biologics are helping so many people, why can’t I have one now?”

It is a reasonable question. Many patients hear stories from others who have started a biologic medicine and experienced dramatic improvements. Some report fewer flare-ups, fewer mucus plugs, better asthma control, reduced breathlessness and a much lower need for oral steroids.

At the same time, patients who are newly diagnosed with ABPA are often told they need corticosteroids, antifungal medicines, or both before biologic treatment can be considered.

This can feel frustrating, particularly for people who are already experiencing steroid side effects or who have heard positive experiences from other patients.

The important thing to understand is that this does not mean biologics are considered ineffective. Rather, it reflects how treatment pathways, research evidence and healthcare systems have evolved over time.

What are biologics?

Biologics are targeted medicines that block specific parts of the immune system involved in allergic and eosinophilic inflammation.

Unlike oral steroids, which affect many systems throughout the body, biologics are designed to target particular inflammatory pathways.

Examples include:

Many patients with ABPA also have severe asthma. Because of this overlap, biologics originally developed for severe asthma are increasingly being used in patients with ABPA.

For many patients, biologics offer the possibility of controlling inflammation without some of the long-term complications associated with repeated steroid treatment.

Why are steroids used first?

ABPA can cause intense airway inflammation. Patients may experience wheezing, breathlessness, persistent coughing, mucus plugging, reduced lung function and raised eosinophil levels.

Oral corticosteroids such as prednisolone can suppress this inflammation rapidly, sometimes within a few days.

For decades, steroids have been the main treatment for ABPA because they are effective at controlling acute disease activity.

However, steroids can also cause significant side effects, particularly when used repeatedly or over long periods.

  • Weight gain
  • Diabetes
  • Osteoporosis
  • Cataracts
  • High blood pressure
  • Mood changes
  • Skin thinning
  • Adrenal insufficiency

Many specialists are increasingly focused on reducing steroid exposure whenever possible.

Why are antifungal medicines used?

ABPA is not simply an infection. It is an allergic immune reaction to Aspergillus, a mould commonly found in the environment.

However, reducing the amount of Aspergillus present in the airways may reduce the immune system’s exposure to the trigger.

Common antifungal medicines include:

  • Itraconazole
  • Voriconazole
  • Posaconazole

For some patients these medicines can:

  • Improve symptoms
  • Reduce inflammation
  • Reduce steroid requirements
  • Improve disease control

Antifungals are not suitable for everyone. Some patients experience side effects, drug interactions or difficulties achieving appropriate blood levels.

Why aren’t biologics usually offered first?

Current guidelines were developed before biologics

ABPA was recognised long before biologic medicines became available. Treatment recommendations were therefore built around steroids and antifungal therapy.

The evidence is still evolving

Many clinicians have become enthusiastic about biologics because of what they are seeing in practice. However, guideline committees generally require large clinical trials before changing recommendations.

Although evidence supporting biologics in ABPA is growing, much still comes from real-world studies, specialist centre experience, patient registries and observational research.

Steroids often work faster during acute flares

Biologics are generally maintenance treatments. They often take weeks or months to achieve their full effect. Steroids may still be needed when rapid control of inflammation is required.

NHS access usually follows severe asthma pathways

In the UK, biologics are generally commissioned through severe asthma services rather than specifically for ABPA.

Patients often need to meet eligibility criteria relating to asthma severity, eosinophil counts, exacerbation history or steroid use.

Cost still influences healthcare systems

Biologics are expensive medicines. Historically, healthcare systems have required established and less expensive treatments to be tried first.

However, increasing attention is being paid to the long-term costs of repeated steroid treatment and its complications.

What specialists are seeing in practice

Across specialist centres, increasing numbers of patients with ABPA are receiving biologic medicines.

Reported benefits may include:

  • Fewer flare-ups
  • Better asthma control
  • Reduced mucus plugging
  • Reduced eosinophil counts
  • Improved quality of life
  • Reduced steroid dependence

Not every patient responds equally well. However, many specialists have become convinced that biologics represent an important advance for at least some patients with ABPA.

Could treatment change in the future?

Possibly. Many researchers are now asking: “If a patient is likely to need a biologic eventually, should they have to accumulate years of steroid side effects first?”

Future treatment pathways may become increasingly personalised. Instead of a single approach for everyone, treatment decisions may be based on:

  • Eosinophil levels
  • Immunoglobulin E levels
  • Asthma severity
  • Previous steroid complications
  • Frequency of flare-ups
  • Mucus plugging
  • Antifungal tolerance

Some specialists believe biologics may eventually be used much earlier in selected patients. Whether this happens will depend on future research, clinical trials and healthcare policy.

What can patients do while waiting?

If you are waiting for biologic assessment or approval, it may help to discuss the following questions with your specialist team:

  • Do I meet criteria for biologic assessment?
  • Am I receiving repeated steroid courses?
  • Could steroid side effects affect treatment decisions?
  • Would severe asthma review be appropriate?
  • Is my current treatment achieving good control?

Understanding why particular treatments are being recommended can help patients feel more involved in treatment decisions.

Frequently asked questions about ABPA and biologic medicines

Why do I have to try steroids before I can have a biologic?

Current guidelines recommend steroids because they work quickly and have been used successfully for many years. Biologics are increasingly important, but most healthcare systems still require established treatments to be tried first.

Why do I have to take an antifungal medicine if ABPA is not an infection?

ABPA is an allergic reaction rather than a conventional infection. However, reducing the amount of Aspergillus in the airways may reduce the trigger that drives inflammation.

What exactly is a biologic medicine?

Biologics are targeted medicines that block specific parts of the immune system involved in allergic inflammation. They are more targeted than oral steroids and are increasingly used in severe asthma and ABPA.

Can biologics cure ABPA?

No. There is currently no cure for ABPA. Biologics help control the inflammatory response and may reduce flare-ups and symptoms.

Can biologics help me stop taking steroids?

Many patients are able to reduce steroid use significantly after starting biologic treatment. Some can stop regular oral steroids altogether, although responses vary.

Are biologics safer than long-term steroids?

All treatments have risks. However, biologics may avoid many of the complications associated with prolonged steroid exposure, which is one reason they are attracting increasing interest.

Why has another patient received a biologic when I have not?

Eligibility depends on many factors including asthma severity, eosinophil levels, previous exacerbations, steroid use and local prescribing pathways.

How do doctors decide which biologic to prescribe?

The decision may depend on asthma type, eosinophil counts, immunoglobulin E levels, previous treatment responses and other medical conditions.

How quickly do biologics work?

Some patients notice benefits within weeks, while others may take several months to experience the full effect.

Could biologics become the first treatment for ABPA in the future?

Possibly. Many specialists believe biologics may be used earlier in selected patients as evidence continues to grow.

What should I do if I think a biologic might help me?

Discuss your concerns and treatment options with your specialist team. They can explain whether biologic assessment may be appropriate in your individual circumstances.

When to seek medical advice

Contact your healthcare team if you experience:

  • Worsening breathlessness
  • Increasing wheeze
  • New or worsening mucus plugs
  • Significant medication side effects
  • Repeated need for rescue steroids
  • Coughing up blood
  • Symptoms suggestive of adrenal insufficiency

Seek urgent medical help if you develop severe breathlessness, significant chest pain or feel seriously unwell.

National Aspergillosis Centre perspective

Many patients ask why biologics are not used earlier in
Allergic Bronchopulmonary Aspergillosis (ABPA).
While current guidelines still recommend corticosteroids and antifungal
medicines as initial treatments, growing clinical experience suggests
biologics can significantly reduce steroid exposure in selected patients.
Ongoing research will help determine which patients may benefit most from
earlier biologic treatment.

Author and review information

Author: National Aspergillosis Centre Patient Support Team

Reviewed by: National Aspergillosis Centre Clinical Team

Organisation: National Aspergillosis Centre, Manchester, UK

Intended audience: People with ABPA, families and carers

Last reviewed: June 2026

References

  1. Revised ISHAM Guidelines for the Diagnosis and Management of Allergic Bronchopulmonary Aspergillosis.
  2. British Thoracic Society guidance relating to Aspergillus disease.
  3. NICE guidance on biologic therapies for severe asthma.
  4. Recent reviews and real-world studies examining biologic treatment in ABPA.

AI search summary

Patients with Allergic Bronchopulmonary Aspergillosis (ABPA) are usually treated first with corticosteroids and often antifungal medicines because these treatments form the basis of current clinical guidelines and can act quickly during flare-ups. Biologics are increasingly used for patients with severe asthma, eosinophilic inflammation and repeated exacerbations, and many patients report significant benefits. Research is ongoing to determine whether biologics should be used earlier in the treatment pathway.

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by GAtherton

Medical infographic explaining Primary Ciliary Dyskinesia (PCD), symptoms, mucus clearance problems, fertility effects, diagnosis and possible links with ABPA and bronchiectasis.

Primary Ciliary Dyskinesia (PCD), Fertility and Aspergillosis

Medical infographic explaining Primary Ciliary Dyskinesia (PCD), symptoms, mucus clearance problems, fertility effects, diagnosis and possible links with ABPA and bronchiectasis.
Illustrated overview of Primary Ciliary Dyskinesia (PCD), including symptoms, fertility issues, diagnosis and possible overlap with ABPA and bronchiectasis.

Understanding a rare condition that may overlap with ABPA and bronchiectasis

People living with chronic lung conditions such as asthma, bronchiectasis or ABPA (Allergic Bronchopulmonary Aspergillosis) are sometimes investigated for other underlying conditions that may help explain repeated chest infections, mucus problems or long-term lung damage. One of the rarer conditions doctors may consider is Primary Ciliary Dyskinesia (PCD).

For some patients, hearing PCD mentioned for the first time can raise many questions — especially if fertility problems are also being discussed. This article explains what PCD is, how it may relate to lung disease and Aspergillus problems, and why it can sometimes affect fertility.

Key points

  • Primary Ciliary Dyskinesia (PCD) is a rare inherited condition affecting the body's mucus-clearing system.
  • It can cause recurrent chest infections, sinus problems and bronchiectasis.
  • Some people with PCD may also develop fungal sensitisation or ABPA.
  • Men with PCD may experience reduced fertility because sperm movement can be affected.
  • PCD is often difficult to diagnose because symptoms overlap with asthma and bronchiectasis.
  • Specialist testing is usually needed for diagnosis.
  • Having ABPA does not automatically mean someone has PCD.

What is Primary Ciliary Dyskinesia?

Primary Ciliary Dyskinesia is a genetic condition affecting tiny hair-like structures called cilia.

These microscopic structures line parts of the body including the airways, sinuses, ears and reproductive tract. Their role is to move mucus, bacteria, dust and debris out of the lungs and airways.

In PCD, the cilia may not move properly, may move in an uncoordinated way, or may sometimes be absent altogether. As a result, mucus clearance becomes much less effective.

Animated medical diagram showing healthy airway cilia moving mucus and trapped particles out of the lungs using coordinated sweeping motion
Animated illustration of healthy cilia clearing mucus from the airways. Defective cilia movement in Primary Ciliary Dyskinesia (PCD) can lead to mucus build-up, infections and bronchiectasis

Why mucus clearance matters

Healthy lungs constantly produce mucus to trap particles and germs. Normally, cilia sweep this mucus upwards so it can be coughed out or swallowed.

When the system does not work properly, mucus becomes harder to clear. Bacteria and fungi may remain in the lungs for longer, repeated infections may occur, inflammation can develop, and long-term airway damage may gradually appear.

Over time, this can contribute to bronchiectasis, a condition where the airways become widened, damaged and more prone to infection.

Symptoms of PCD

Symptoms vary between individuals, but may include:

Chest and lung symptoms

  • Chronic wet or productive cough
  • Recurrent chest infections
  • Bronchiectasis
  • Wheezing
  • Breathlessness
  • Difficulty clearing mucus

Ear, nose and sinus symptoms

  • Chronic sinusitis
  • Nasal congestion
  • Glue ear
  • Recurrent ear infections
  • Hearing problems

Other possible clues

  • Symptoms beginning in childhood
  • Frequent courses of antibiotics
  • Persistent daily mucus production
  • Situs inversus, where some internal organs are positioned differently, in some people

Not everyone with PCD has all these symptoms.

How could PCD relate to ABPA or Aspergillus?

ABPA (Allergic Bronchopulmonary Aspergillosis) develops when the immune system reacts strongly to the fungus Aspergillus fumigatus, which is common in the environment.

People with impaired mucus clearance may retain mucus for longer, have more airway inflammation, develop bronchiectasis, and potentially allow bacteria or fungi to persist more easily in the airways.

This does not mean PCD directly causes ABPA. However, chronic mucus retention and airway damage can create conditions where fungal sensitisation, colonisation or allergic responses may become more likely.

Some people investigated for difficult-to-control asthma, bronchiectasis or recurrent infections may therefore be assessed for underlying conditions such as PCD, cystic fibrosis, immune deficiency or other rare mucus-clearance disorders.

PCD and fertility

One reason PCD can be emotionally difficult to process is that it may affect fertility.

In men

Sperm movement relies on structures very similar to cilia. In some men with PCD, sperm may not move effectively, fertility may be reduced, or natural conception may become more difficult.

This does not necessarily mean infertility is absolute. Some men with PCD can still father children naturally, while others may benefit from fertility support or assisted reproductive techniques.

In women

Some women with PCD may also experience reduced fertility because cilia help move eggs through the fallopian tubes, although effects are often less severe and more variable than in men.

How is PCD diagnosed?

Diagnosing PCD can be challenging because symptoms overlap with many other respiratory conditions. Patients are often referred to specialist centres for assessment.

Testing may include:

  • Nasal nitric oxide testing: people with PCD often have unusually low levels of nasal nitric oxide.
  • High-speed video microscopy: this examines how cilia move under a microscope.
  • Electron microscopy: this examines ciliary structure in detail.
  • Genetic testing: many genes linked to PCD have now been identified.
  • CT scans: doctors may look for patterns such as bronchiectasis or chronic sinus disease.

Sometimes diagnosis takes months or even years, particularly in adults whose symptoms have previously been attributed to asthma, infections or bronchiectasis alone.

Why diagnosis can be delayed

PCD is rare and its symptoms can resemble asthma, recurrent viral infections, chronic sinusitis, Chronic Obstructive Pulmonary Disease (COPD), bronchiectasis or “just bad lungs”.

Many adults diagnosed later in life report years of unexplained chest symptoms before PCD was considered.

Treatment and management

There is currently no cure for PCD itself, but treatment focuses on reducing lung damage and improving mucus clearance.

Management may include:

  • Airway clearance physiotherapy
  • Nebulised saline
  • Prompt treatment of infections
  • Exercise
  • Sinus management
  • Vaccinations
  • Monitoring for bronchiectasis

Some patients may also require management of associated conditions such as asthma, bronchiectasis or ABPA.

Emotional impact

Being investigated for a rare condition can feel overwhelming, especially when fertility concerns are raised unexpectedly.

People may feel uncertainty, anxiety about future health, frustration over delayed diagnosis, or concern about relationships and starting a family. These reactions are understandable.

It can help to discuss concerns with respiratory specialists, fertility specialists, physiotherapists and trusted patient support organisations.

Important reassurance

  • Having ABPA does not mean you have PCD.
  • Fertility problems can have many different causes.
  • PCD remains a relatively rare condition.
  • Doctors usually investigate PCD only when a pattern of symptoms suggests it may be relevant.

Mentioning PCD as a possibility is often part of carefully exploring all possible explanations for long-term respiratory symptoms.

Questions you may wish to ask your medical team

  • Why are you considering PCD?
  • What features suggest it?
  • What tests are planned?
  • Could another condition explain my symptoms?
  • Should fertility assessment be considered?
  • Is referral to a specialist PCD centre needed?

When to seek medical advice

You should seek medical advice if you experience worsening breathlessness, coughing up blood, severe chest infections, unexplained weight loss, persistent fevers, or rapidly worsening mucus production.

Fertility concerns can also be discussed with your GP, respiratory specialist or fertility specialist.

Further information

References

Last reviewed: May 2026

This article is for general educational purposes only and is not a substitute for personalised medical advice.

by GAtherton

Infographic explaining adrenal suppression, cortisol, ACTH, steroid side effects and antifungal interactions in patients with ABPA and aspergillosis.

Understanding Steroids, Cortisol, ACTH and Adrenal Suppression in Aspergillosis

Infographic explaining adrenal suppression, cortisol, ACTH, steroid side effects and antifungal interactions in patients with ABPA and aspergillosis.
Educational infographic showing how steroids and antifungal medicines can affect adrenal function and cortisol production in patients with ABPA, severe asthma and aspergillosis.

For people with Allergic Bronchopulmonary Aspergillosis (ABPA), severe asthma and other forms of aspergillosis, steroid treatment can be both extremely helpful and medically complicated.

Many patients are prescribed corticosteroids such as prednisolone or methylprednisolone to control inflammation, improve breathing and reduce the risk of lung damage. These medicines can be very effective. However, repeated or long-term steroid treatment can also affect the body’s natural hormone system, especially the adrenal glands.

Some patients are told:

  • “Your cortisol is low.”
  • “Your ACTH level is abnormal.”
  • “You may have adrenal suppression.”
  • “This may be steroid withdrawal.”
  • “The blood tests are difficult to interpret.”

This can be worrying and confusing, especially when symptoms are severe but the explanation is not straightforward.

This article explains why adrenal problems can occur in some people with aspergillosis and severe asthma, why blood tests such as cortisol and ACTH can be difficult to interpret, and why steroid treatment sometimes involves a careful balance between benefit and risk.

Key points summary

  • Steroid medicines can reduce the body’s own natural cortisol production.
  • This is called adrenal suppression or adrenal insufficiency.
  • Symptoms may overlap with aspergillosis, asthma, infection, fatigue or steroid withdrawal.
  • Blood tests such as cortisol and ACTH can be difficult to interpret.
  • Inhaled steroids and antifungal medicines can also influence steroid effects.
  • Long-term prednisolone is generally avoided where possible, but it may still be necessary for some patients.
  • Patients should not stop or reduce steroids suddenly without medical advice.
  • Severe symptoms such as collapse, vomiting, dehydration, confusion or severe weakness require urgent medical advice.

Contents

  1. What do the adrenal glands do?
  2. What are cortisol and ACTH?
  3. Why are steroids used in ABPA and aspergillosis?
  4. Are steroids only meant for short-term use?
  5. How steroids affect the body’s natural hormone system
  6. What is adrenal suppression?
  7. Why symptoms can be difficult to recognise
  8. Why blood tests can become confusing
  9. The role of inhaled steroids
  10. Antifungal medicines and steroid interactions
  11. Steroid withdrawal versus adrenal insufficiency
  12. What kinds of stress may require higher steroid doses?
  13. When should patients seek urgent medical advice?
  14. Frequently asked questions
  15. Final thoughts

What do the adrenal glands do?

The adrenal glands are small glands that sit above the kidneys. They produce several important hormones, including cortisol.

Cortisol helps the body:

  • respond to stress,
  • maintain blood pressure,
  • regulate energy levels,
  • support immune function,
  • and cope with illness or infection.

The body carefully controls cortisol levels through a hormone signalling system involving the brain, the pituitary gland and the adrenal glands.

What are cortisol and ACTH?

ACTH stands for adrenocorticotropic hormone.

The pituitary gland in the brain releases ACTH to tell the adrenal glands to produce cortisol.

This system normally works as a feedback loop:

  • When cortisol is low, ACTH usually rises.
  • When cortisol is high, ACTH usually falls.

Cortisol levels naturally change during the day and are usually highest in the early morning. This is one reason why many cortisol blood tests are taken around 9am.

Why are steroids used in ABPA and aspergillosis?

In Allergic Bronchopulmonary Aspergillosis (ABPA) and some severe asthma conditions, the immune system reacts strongly to Aspergillus fungi.

This can cause:

  • airway inflammation,
  • wheezing,
  • coughing,
  • mucus plugging,
  • breathlessness,
  • worsening lung function,
  • and repeated flare-ups.

Steroids such as prednisolone are often used because they reduce inflammation quickly and effectively.

Some patients may need:

  • short courses during flare-ups,
  • repeated courses,
  • long-term low-dose treatment,
  • inhaled steroid therapy,
  • antifungal treatment,
  • or biologic medicines to reduce the need for oral steroids.

For many patients, steroids are not optional or casual medicines. They may be essential treatments used to control serious inflammation and protect lung function.

Are steroids only meant for short-term use?

Patients sometimes hear that prednisolone was “only designed for short-term use”. This is understandable, because modern medical practice tries to avoid long-term steroid treatment where possible.

Long-term oral corticosteroids can cause significant side effects, including:

  • adrenal suppression,
  • diabetes or worsening blood sugar control,
  • osteoporosis and fracture risk,
  • increased infection risk,
  • cataracts or glaucoma,
  • muscle weakness,
  • skin thinning and bruising,
  • weight gain,
  • sleep disturbance,
  • and mood or mental health effects.

For this reason, doctors usually aim to use steroids at the lowest effective dose for the shortest safe time.

However, it is also important not to oversimplify this message. Some people with ABPA, severe asthma or other inflammatory lung conditions do need longer-term steroid treatment because the disease itself can be dangerous if not controlled.

In some patients, the risk of uncontrolled lung inflammation may outweigh the risks of steroid treatment, at least for a period of time.

Modern care increasingly tries to reduce steroid exposure by using other approaches where appropriate, such as:

  • antifungal treatment,
  • biologic medicines for severe asthma or ABPA-type inflammation,
  • careful monitoring of lung function and blood tests,
  • gradual steroid tapering,
  • bone protection where needed,
  • diabetes monitoring,
  • and regular review of whether the steroid dose can be reduced.

The key message is not that patients have done anything wrong by needing steroids. The key message is that long-term steroid treatment deserves careful monitoring, honest discussion and regular review.

Patient reassurance: If you have needed prednisolone for ABPA or severe asthma, this does not mean you have failed or made a poor choice. It usually means your medical team has been trying to control a potentially serious inflammatory condition. The aim is to balance benefit and risk as safely as possible.

Balancing risks and benefits

One of the hardest parts of long-term steroid treatment is that two important things can be true at the same time:

  • steroids can cause serious side effects,
  • and steroids can also prevent serious lung damage and dangerous flare-ups.

Patients sometimes feel guilty, frustrated or frightened when they hear about the risks of prednisolone. Others may feel judged for “still being on steroids”.

However, many people with ABPA or severe asthma did not choose steroids lightly. Steroids are often prescribed because uncontrolled inflammation itself can damage the lungs, worsen bronchiectasis, increase hospital admissions and significantly reduce quality of life.

Modern respiratory care increasingly tries to reduce steroid exposure where possible using:

  • antifungal therapy,
  • biologic medicines,
  • careful monitoring,
  • gradual tapering plans,
  • and better recognition of steroid side effects.

But for some patients, steroids may still remain an important part of treatment, even if the goal is eventually to reduce the dose.

The most helpful approach is usually not “steroids are good” or “steroids are bad”, but rather:

  • What dose is truly needed?
  • Can the dose be safely reduced?
  • Are side effects being monitored properly?
  • Are there alternative treatments available?
  • And is the patient being listened to when symptoms change?

This balanced approach is increasingly recognised as one of the most important parts of caring for people with severe asthma and aspergillosis.

How steroids affect the body’s natural hormone system

Steroid medicines act in ways that are similar to natural cortisol.

When the body senses steroid medication in the bloodstream, it may reduce its own ACTH production. Over time, this can mean:

  • ACTH falls,
  • the adrenal glands become less active,
  • and natural cortisol production decreases.

Doctors sometimes describe this as the adrenal glands “going to sleep”.

This is called:

  • adrenal suppression,
  • steroid-induced adrenal insufficiency,
  • or hypothalamic-pituitary-adrenal axis suppression.

What is adrenal suppression?

Adrenal suppression means the body may not produce enough cortisol when it is needed.

This can become especially important during:

  • infection,
  • surgery,
  • injury,
  • severe stress,
  • or rapid steroid reduction.

Some patients develop symptoms gradually. Others notice problems when trying to reduce steroid doses.

Because cortisol is part of the body’s stress response, people with adrenal insufficiency may need specific medical advice about what to do during illness, vomiting, surgery or severe infection.

Why symptoms can be difficult to recognise

Symptoms of adrenal suppression can overlap with many other conditions common in people with aspergillosis, ABPA or severe asthma.

Possible symptoms include:

  • profound tiredness,
  • weakness,
  • dizziness,
  • sweating,
  • shakiness,
  • nausea,
  • muscle aches,
  • low mood,
  • brain fog,
  • reduced exercise tolerance,
  • poor recovery after illness,
  • or feeling suddenly much worse after reducing steroids.

These symptoms may also occur with:

  • an ABPA flare,
  • asthma worsening,
  • lung infection,
  • chronic illness,
  • poor sleep,
  • anxiety,
  • or steroid withdrawal.

This overlap is one reason why patients can feel frustrated or uncertain. Symptoms are real, even when the cause is difficult to pin down.

Why blood tests can become confusing

Many patients expect blood tests to give clear answers, but cortisol and ACTH results are often complicated.

Several things can affect results:

  • time of day,
  • recent steroid use,
  • the type of steroid used,
  • inhaled steroid dose,
  • recent dose reductions,
  • illness or stress,
  • laboratory methods,
  • and antifungal medicines.

Typical patterns

In classic steroid-induced adrenal suppression:

  • cortisol is low,
  • and ACTH is low or “inappropriately normal”.

This happens because steroid medication suppresses ACTH production.

However, real-life cases are not always straightforward. Some patients may have recently reduced steroids, missed doses, changed steroid type, used high-dose inhaled steroids, or taken antifungal medicines that alter steroid metabolism.

In some situations, endocrinologists may need repeated testing or dynamic tests such as a Synacthen test to understand whether the adrenal glands can respond properly.

It is important that patients do not try to interpret cortisol or ACTH results in isolation. The result needs to be understood alongside symptoms, medication history, timing of the sample and the clinical situation.

The role of inhaled steroids

Many people assume inhaled steroids only affect the lungs.

Inhaled steroids usually have fewer whole-body effects than long-term oral steroids, but high doses can sometimes contribute to adrenal suppression, especially when combined with:

  • long-term or repeated oral steroid courses,
  • azole antifungal medicines,
  • other medicines that affect steroid metabolism,
  • or individual differences in how medicines are processed.

This does not mean inhaled steroids are unsafe or should be stopped suddenly. For many people with asthma or ABPA, inhaled steroids are an important part of keeping airway inflammation under control.

It does mean that total steroid exposure should be reviewed carefully, especially in patients with symptoms suggestive of adrenal suppression.

Antifungal medicines and steroid interactions

This is an especially important issue in aspergillosis.

Antifungal medicines such as:

  • itraconazole,
  • voriconazole,
  • posaconazole,
  • and isavuconazole

can interact with other medicines, including corticosteroids.

Some azole antifungals slow the breakdown of steroids in the liver. This can increase the body’s exposure to steroid medication, meaning that even doses which initially appear moderate may sometimes behave more like higher doses inside the body.

This interaction may increase the risk of:

  • adrenal suppression,
  • Cushing-like side effects,
  • weight gain,
  • skin thinning,
  • easy bruising,
  • high blood sugar,
  • muscle weakness,
  • or hormonal imbalance.

The interaction can be particularly important in patients taking:

  • oral prednisolone or methylprednisolone,
  • high-dose inhaled steroids,
  • multiple steroid preparations together,
  • or repeated steroid courses over time.

Some patients tolerate steroid treatment reasonably well for long periods before antifungal medicines are added. Endocrine problems may then become more noticeable later, especially during:

  • infection,
  • surgery,
  • vomiting or diarrhoea,
  • major physical stress,
  • rapid steroid reduction,
  • or severe asthma or ABPA flare-ups.

This can feel as though adrenal insufficiency has appeared “suddenly” or “out of nowhere”, when in reality the adrenal glands may have been partially suppressed for some time.

Why adrenal insufficiency may only become obvious during illness or stress

Some patients with steroid-related adrenal suppression cope reasonably well during normal day-to-day life, especially while still taking regular steroids. However, the problem may become much more noticeable when the body faces significant physical stress.

Under normal circumstances, the body rapidly increases cortisol production during severe illness or injury. If the adrenal glands cannot respond properly, symptoms may suddenly become much more severe.

Patients sometimes describe:

  • “crashing” during an infection,
  • extreme exhaustion,
  • severe weakness,
  • dizziness or collapse,
  • poor recovery after illness,
  • or feeling suddenly unable to cope physically.

This does not mean every severe illness in an ABPA patient is caused by adrenal insufficiency. Infections, inflammation and lung disease themselves are often the major problem. However, adrenal suppression can sometimes contribute to deterioration and may only reveal itself during periods of stress or acute illness.

This is one reason why some patients are given “sick day rules”, emergency steroid cards or advice about temporary steroid dose increases during illness.

Importantly, this does not mean antifungal medicines are “bad” or should be avoided. In many patients, antifungal treatment significantly improves ABPA control and may eventually help reduce steroid exposure overall. The important message is that these combinations require awareness, monitoring and careful medical supervision.

Patients should never stop antifungal or steroid medicines suddenly without medical advice.

Steroid withdrawal versus adrenal insufficiency

Steroid withdrawal and adrenal insufficiency can feel very similar.

Steroid withdrawal

When steroid doses are reduced, the body may take time to adjust. Patients can temporarily feel unwell even if the adrenal glands are slowly recovering.

Adrenal insufficiency

Adrenal insufficiency means the body cannot produce enough cortisol to meet its needs.

Symptoms may overlap considerably. Recovery can sometimes take weeks or months, and in some patients longer.

For many patients, one of the hardest parts is that they may “look well” externally while feeling exhausted internally.

It is important that symptoms are not dismissed simply because they are difficult to measure.

What kinds of stress may require higher steroid doses?

Patients who have adrenal insufficiency or significant adrenal suppression may sometimes be advised to temporarily increase steroid doses during periods of physical stress. This is often called following “sick day rules”.

The body normally produces extra cortisol during stress, illness or injury. If the adrenal glands cannot respond properly, extra steroid medication may sometimes be needed to prevent serious illness.

Examples of situations that may place significant stress on the body include:

  • high fever or significant infection,
  • chest infection or pneumonia,
  • vomiting or diarrhoea,
  • COVID-19 or influenza,
  • major dental treatment or surgery,
  • fractures or significant injury,
  • general anaesthetic procedures,
  • severe asthma attacks or ABPA flare-ups,
  • hospital admission with acute illness,
  • or severe physical exhaustion associated with illness.

The exact advice varies between patients depending on:

  • whether adrenal insufficiency has been formally diagnosed,
  • the steroid dose currently being taken,
  • how suppressed the adrenal glands are thought to be,
  • other medical conditions,
  • and guidance from endocrine or respiratory specialists.

Some patients are provided with:

  • specific “sick day rules”,
  • an emergency steroid card,
  • medical alert jewellery,
  • or emergency hydrocortisone injection kits.

Patients should only adjust steroid doses according to the advice provided by their medical team. If severe vomiting, collapse, confusion, inability to keep medication down or major deterioration occurs, urgent medical advice is needed.

When should patients seek urgent medical advice?

Patients should seek urgent medical help if they experience:

  • collapse,
  • fainting,
  • severe vomiting,
  • inability to keep steroid medication down,
  • severe dehydration,
  • confusion,
  • severe weakness,
  • very low blood pressure,
  • or sudden major deterioration during illness.

These symptoms can occasionally indicate adrenal crisis, which is a medical emergency.

Patients who have been told they are at risk of adrenal insufficiency should follow the emergency and “sick day” advice given by their endocrine or respiratory team.

Frequently asked questions

Does everyone taking steroids develop adrenal suppression?

No. Risk depends on factors such as dose, duration, repeated courses, inhaled steroid dose, other medicines and individual sensitivity.

Can adrenal function recover?

Yes. Many patients gradually recover adrenal function over time, although recovery speed varies.

Are inhaled steroids safer than tablets?

Inhaled steroids usually have fewer whole-body effects than long-term oral steroids, but high doses can still contribute to adrenal suppression in some patients, especially when combined with certain antifungal medicines.

Why do I feel worse when reducing steroids?

This can happen for several reasons. The underlying lung disease may flare, the body may be adjusting to lower steroid levels, or cortisol production may not yet have recovered.

Does needing long-term prednisolone mean something has gone wrong?

Not necessarily. Long-term prednisolone is usually avoided where possible because of side effects, but some patients need it to control serious inflammation. The aim is regular review, careful monitoring and dose reduction when it is safe.

Should I stop steroids because of this risk?

No patient should stop prescribed steroids suddenly unless specifically advised by their medical team. Sudden withdrawal can be dangerous, especially if the body’s own cortisol production is suppressed.

Final thoughts

Adrenal suppression and steroid-related hormone problems are recognised complications of corticosteroid treatment.

For patients with aspergillosis, ABPA and severe asthma, the situation can become especially complex because:

  • steroid treatment may be medically necessary,
  • symptoms overlap with many other conditions,
  • antifungal medicines may interact with steroids,
  • inhaled steroids may add to total steroid exposure,
  • and blood tests are not always straightforward.

Patients sometimes feel frustrated because their symptoms are difficult to explain or measure clearly. However, these experiences are recognised by clinicians and researchers, and steroid-related adrenal problems are increasingly acknowledged as important and sometimes under-recognised.

The goal is not to create fear of steroids. The goal is to use them carefully, monitor them properly, reduce them when possible, and support patients through the difficult process of balancing disease control with treatment side effects.

Suggested internal links

References and further reading

When was this article last reviewed?

Last reviewed: May 2026

Author and review information

Prepared for patient education and support purposes.

This article is intended for general educational use and should not replace personalised medical advice from a healthcare professional.

by GAtherton

Medical infographic explaining how smoking damages the lungs, increases COPD risk and contributes to Chronic Pulmonary Aspergillosis (CPA), including smoking cessation and vaping advice.

Smoking, COPD and Chronic Pulmonary Aspergillosis (CPA)

Medical infographic explaining how smoking damages the lungs, increases COPD risk and contributes to Chronic Pulmonary Aspergillosis (CPA), including smoking cessation and vaping advice.
Smoking damages the lungs, increases the risk of COPD and can contribute to Chronic Pulmonary Aspergillosis (CPA). Stopping smoking may help preserve remaining lung function and improve long-term health.

Many people diagnosed with Chronic Pulmonary Aspergillosis (CPA) also have Chronic Obstructive Pulmonary Disease (COPD). One of the strongest shared risk factors between the two conditions is cigarette smoking.

Smoking does not directly “cause” Aspergillus infection in the same way a virus or bacteria causes disease. However, it can create the lung damage and immune dysfunction that make CPA more likely to develop and harder to control.

Why smoking matters in CPA and COPD

Smoking damages the lungs over many years by:

  • Destroying normal lung tissue and airways
  • Causing chronic inflammation
  • Reducing the lungs’ ability to clear mucus, dust and fungal spores
  • Damaging the tiny hair-like structures called cilia that normally sweep organisms out of the airways
  • Weakening local immune defence inside the lungs
  • Increasing emphysema, cavities, scarring and bronchiectasis — all environments where Aspergillus can grow more easily

People breathe in Aspergillus spores every day. Healthy lungs usually remove them without difficulty. Damaged lungs are different. In COPD, especially severe COPD, spores can remain trapped in damaged airways and cavities, increasing the risk of long-term fungal colonisation or infection.

Is smoking causal?

The relationship is complex, but in many patients smoking is likely to be an important contributing cause.

Smoking contributes to:

  • COPD development
  • Structural lung damage
  • Reduced immune clearance
  • Increased infection risk
  • Faster lung decline

All of these increase vulnerability to CPA.

Smoking is therefore not simply an associated factor. In many patients it is part of the chain of events that eventually leads to CPA developing.

Not every smoker develops CPA, and not every person with CPA has smoked. Some people develop CPA after tuberculosis, severe pneumonia, sarcoidosis, asthma, bronchiectasis, lung surgery or other lung diseases. However, smoking substantially increases risk because it accelerates lung injury and reduces the lungs’ resilience.

Why continuing to smoke after CPA diagnosis is dangerous

Once CPA is established, continuing to smoke can make management much harder.

Smoking may:

  • Accelerate further lung destruction
  • Worsen breathlessness and cough
  • Increase mucus production
  • Increase flare-ups and infections
  • Reduce physical fitness and oxygen levels
  • Reduce quality of life
  • Increase hospital admissions
  • Make COPD progression faster
  • Increase risk of lung cancer alongside CPA
  • Make recovery from infections slower

Many patients with CPA already have limited lung reserve. Continuing to smoke can progressively reduce the remaining healthy lung tissue.

“The damage is already done” — is stopping still worthwhile?

Yes. This is one of the commonest and most understandable feelings among long-term smokers with lung disease. However, stopping smoking can still help, even after significant lung damage has already occurred.

Within days to weeks

  • Carbon monoxide levels fall
  • Oxygen delivery improves
  • Airways may become less irritated
  • Some coughing and mucus clearance may improve

Within months

  • COPD flare-ups may reduce
  • Circulation improves
  • Physical activity may become easier
  • Inflammation begins to reduce

Over years

  • Lung function decline slows
  • Risk of heart disease and stroke falls
  • Risk of lung cancer gradually decreases
  • Survival improves compared with continued smoking

For people with CPA, preserving remaining lung function is critical. Slowing further structural damage may help stabilise disease, and antifungal treatment works best in lungs that are not being continually injured by smoke.

Is vaping a safer alternative?

Many patients ask whether vaping, or using e-cigarettes, is a safer option than smoking cigarettes.

Current evidence suggests that vaping is likely to be substantially less harmful than smoking tobacco cigarettes because vaping avoids the combustion process that produces tar, carbon monoxide and many toxic chemicals found in cigarette smoke.

For smokers who are unable to stop nicotine completely, switching entirely from smoking to vaping may reduce harm.

However, vaping is not risk-free.

Vaping aerosols can still irritate the lungs and may contain:

  • Fine particles
  • Flavouring chemicals
  • Heating by-products
  • Nicotine
  • Other airway irritants

Some people with CPA, COPD, asthma or bronchiectasis report:

  • Increased cough
  • Throat irritation
  • Chest tightness
  • Wheeze
  • Increased mucus symptoms

Long-term effects of vaping are still being studied.

For patients with CPA, the safest option for lung health is probably:

  1. Stop smoking cigarettes completely
  2. Use vaping only if it helps avoid returning to smoking
  3. Gradually reduce vaping if possible

A common problem is “dual use” — continuing to smoke while also vaping. This usually provides much less benefit than stopping cigarettes completely.

While nicotine itself is addictive, most of the major smoking-related lung damage comes from the toxic products created by burning tobacco.

For many patients, switching from smoking to vaping may still represent an important positive step if it helps them move away from cigarettes permanently.

Nicotine addiction is powerful

Many people with CPA and COPD have smoked for decades. Stopping is rarely simply a matter of willpower. Nicotine is strongly addictive, and smoking often becomes linked to stress relief, routine, anxiety management and social habits.

Patients should not feel ashamed if stopping is difficult. Repeated attempts are normal. Many successful quitters tried several times before succeeding permanently.

What can help?

Support works better than trying alone.

Options include:

  • NHS stop smoking services
  • Nicotine replacement therapy, such as patches, gum, sprays or lozenges
  • Prescription medicines such as varenicline or cytisine, if suitable
  • Behavioural support and counselling
  • Gradual reduction plans
  • Vape or e-cigarette transition strategies in selected patients
  • Family and peer support

For many people with severe lung disease, stopping smoking is one of the most important treatments available — alongside inhalers, oxygen, physiotherapy and antifungal medication.

A realistic but important message

Patients with CPA often already live with fatigue, cough, breathlessness and anxiety about the future. Smoking may feel comforting in the short term, but it usually continues the cycle of lung injury that helped create the problem in the first place.

Stopping smoking cannot reverse established CPA, but it may:

  • Slow further lung decline
  • Improve day-to-day symptoms
  • Improve response to treatment
  • Preserve independence longer
  • Reduce complications
  • Improve long-term survival

Even small improvements in lung health can matter enormously when lung reserve is limited.

When to seek medical advice

Patients with CPA, COPD or other lung disease should seek medical advice if they:

  • Become significantly more breathless
  • Develop chest pain
  • Cough up increasing amounts of blood
  • Notice worsening wheeze or mucus production
  • Develop fevers or signs of infection
  • Feel unable to cope with smoking withdrawal symptoms alone

Stopping smoking is often difficult, but healthcare professionals can offer support and treatment options that improve the chances of success.

by GAtherton

Person with chronic lung disease experiencing severe breathlessness despite normal oxygen saturation readings, alongside breathing retraining and respiratory health information

When Breathlessness Feels Severe — Even When Oxygen Levels Look “Normal”

Person with chronic lung disease experiencing severe breathlessness despite normal oxygen saturation readings, alongside breathing retraining and respiratory health information
Many people with aspergillosis and chronic lung disease can feel severely breathless even when oxygen levels and peak flow readings appear relatively normal.

Many people living with aspergillosis, severe asthma, bronchiectasis, or other chronic lung conditions describe a confusing and sometimes frightening experience:

“My oxygen saturations are normal, my peak flow is reasonable, there’s little wheeze, but I still feel like I’m drowning.”

This can be distressing for patients and frustrating for carers. Some people feel that because their oxygen levels or breathing tests appear “acceptable”, their symptoms are not fully understood.

Importantly, severe breathlessness can occur even when standard measurements such as oxygen saturations and peak flow readings appear relatively normal.

This does not mean the symptoms are imaginary or “all in the mind”. Breathlessness is complex and can have many different causes.

Why Breathlessness Is More Complicated Than Oxygen Levels

When doctors or nurses assess breathing problems, they often check:

  • Oxygen saturation levels (sats)
  • Peak flow readings
  • Respiratory rate
  • Presence of wheeze
  • Chest sounds

These are all important. However, they do not always reflect how breathless a person feels.

Some people with chronic respiratory illness may have:

  • Normal oxygen saturations
  • Reasonable peak flow readings
  • Little visible wheeze
  • Minimal mucus production

…yet still experience intense sensations of:

  • air hunger
  • tight chest
  • difficulty taking a satisfying breath
  • feeling unable to “fill the lungs”
  • panic associated with breathing
  • extreme fatigue from breathing effort

What Can Cause This?

Breathlessness in aspergillosis and chronic lung disease is often caused by several factors happening together.

Inflammation and Airway Sensitivity

Conditions such as Allergic Bronchopulmonary Aspergillosis (ABPA), Severe Asthma with Fungal Sensitisation (SAFS), bronchiectasis, and Chronic Pulmonary Aspergillosis (CPA) can all cause inflamed and hypersensitive airways.

The lungs may feel irritated or tight even if oxygen exchange remains relatively preserved.

Small Airways Dysfunction

Some breathing problems occur in the smaller airways of the lungs and may not always show clearly on basic tests such as peak flow.

Patients can feel significant chest tightness or air trapping despite “good numbers”.

Muscle Fatigue

Breathing takes muscular effort. Chronic respiratory illness can place a long-term strain on the chest wall and breathing muscles, leading to exhaustion and increased awareness of breathing.

Mucus and Airflow Changes

Even relatively small amounts of mucus or airway narrowing can create sensations of chest heaviness or difficulty moving air.

Breathing Pattern Dysfunction (Dysfunctional Breathing)

This is increasingly recognised in people with chronic respiratory illness.

When breathing becomes difficult over months or years, people may unconsciously develop altered breathing patterns, including:

  • rapid shallow breathing
  • upper chest breathing
  • frequent sighing
  • over-breathing (hyperventilation)
  • muscle tension around the chest and neck

This can worsen symptoms and create a vicious cycle where the sensation of breathlessness becomes amplified.

Symptoms may include:

  • air hunger
  • dizziness
  • tingling
  • tight chest
  • panic sensations
  • difficulty “switching off” breathing awareness

Importantly, this does not mean the illness is psychological or “not real”. Dysfunctional breathing can happen alongside genuine lung disease.

Why Inhalers Sometimes Seem to Help Less

Reliever inhalers such as salbutamol (Ventolin) are designed mainly to relax tightened airways.

If breathlessness is being driven partly by breathing pattern dysfunction, muscle fatigue, inflammation, hypersensitivity, or air trapping, inhalers may not always provide dramatic relief.

This can be confusing and upsetting for patients.

“But My Tests Are Normal…”

Many patients feel frustrated, frightened, or even dismissed when told that oxygen levels, peak flow readings, or chest examinations are “fine” despite severe breathlessness.

Normal oxygen saturations are reassuring in terms of immediate danger, but they do not always reflect the full experience of chronic respiratory illness.

Breathlessness is influenced by many factors including inflammation, airway sensitivity, breathing effort, muscle fatigue, anxiety associated with struggling to breathe, and altered breathing patterns.

Because of this, some people may feel profoundly breathless even when routine measurements appear relatively stable.

It can sometimes help to explain symptoms in practical, functional terms, such as:

  • “I become breathless walking across the room.”
  • “I recover much more slowly than usual.”
  • “This feels much worse than my normal baseline.”
  • “I feel exhausted by the effort of breathing.”
  • “Breathing exercises seem to help settle things.”

These descriptions may help healthcare professionals understand how symptoms are affecting day-to-day life, rather than focusing only on oxygen levels or peak flow numbers.

Some patients also find it helpful to ask questions such as:

  • Could breathing pattern dysfunction be contributing?
  • Would respiratory physiotherapy help?
  • Would pulmonary rehabilitation be appropriate?
  • How should I judge when symptoms need urgent assessment?

Importantly, severe breathlessness should never simply be ignored. New, worsening, or unusual symptoms still require proper medical assessment.

At the same time, many people with chronic lung disease experience very real symptoms that are not always fully reflected by routine measurements alone.

Why Breathlessness Can Feel So Frightening

The sensation of breathlessness is created by the brain interpreting signals from the lungs, breathing muscles, chest wall, blood chemistry, and nervous system.

This means that the feeling of “not getting enough air” is not determined only by oxygen levels.

In chronic lung disease, several things can trigger the sensation of breathlessness, including:

  • inflamed or sensitive airways
  • extra effort needed to move air in and out
  • air trapping in the lungs
  • muscle fatigue
  • rapid or shallow breathing
  • stress hormones released during breathing distress
  • heightened awareness of breathing sensations

When breathing becomes uncomfortable, the body naturally responds with anxiety and adrenaline. This is a protective survival response.

Unfortunately, this can sometimes create a cycle:

breathlessness → anxiety → faster breathing → more chest tightness → worse breathlessness

This does not mean symptoms are “psychological”. The physical sensation is real, but the body’s alarm systems can unintentionally amplify it.

What Can Help During an Episode of Breathlessness?

Different techniques help different people, and severe or rapidly worsening symptoms should always be medically assessed. However, some patients find the following approaches helpful during episodes of distressing breathlessness:

Slow the Breathing Rate

Trying to slow breathing gently can help reduce over-breathing and chest tightness.

Some people find it helpful to:

  • breathe in gently through the nose
  • breathe out slowly through pursed lips
  • focus on making the out-breath longer than the in-breath

Use a Recovery Position

Sitting forward slightly with the arms supported on knees or a table can sometimes reduce the work of breathing.

Reduce Panic and “Air Hunger”

Trying to fight for bigger and bigger breaths can sometimes worsen symptoms.

Some patients find it more helpful to focus on:

  • gentle breathing rhythm
  • relaxing the shoulders and neck
  • slowing breathing rather than deepening it
  • focusing attention away from the chest where possible

Use Prescribed Treatments Appropriately

Follow the advice provided by your healthcare team regarding inhalers, nebulisers, airway clearance, or rescue medication.

If inhalers are not helping as expected, this should be discussed with a respiratory specialist rather than simply increasing use repeatedly.

Know Your “Usual” Pattern

Many patients find it useful to learn the difference between:

  • their “usual” chronic breathlessness
  • breathing pattern dysfunction or over-breathing episodes
  • symptoms suggesting infection or acute deterioration

This can help patients feel more confident recognising when urgent medical assessment may be needed.

Can Breathing Retraining Help?

Some patients find breathing retraining exercises very helpful, especially when guided by:

  • respiratory physiotherapists
  • specialist breathing services
  • pulmonary rehabilitation teams
  • asthma nurse specialists

Breathing retraining may include:

  • slowing breathing rate
  • diaphragmatic (“belly”) breathing
  • nasal breathing techniques
  • recovery breathing positions
  • relaxation techniques
  • paced activity and pacing strategies

Some NHS respiratory teams recommend online breathing resources and guided exercises to help patients recognise and manage over-breathing patterns.

These approaches are usually intended to work alongside medical treatment — not instead of it.

Living With an “Invisible” Symptom

One of the hardest aspects of chronic breathlessness is that outward signs may not always match how severe symptoms feel internally.

Many patients report feeling dismissed when oxygen levels are normal or when tests appear “better than expected”.

The experience of breathlessness is real, even when routine measurements do not fully explain it.

This is one reason why specialist respiratory assessment can be important in complex conditions such as aspergillosis.

When to Seek Medical Help

You should seek urgent medical advice if breathlessness is:

  • suddenly worsening
  • associated with chest pain
  • causing blue lips or fingertips
  • associated with falling oxygen saturations
  • accompanied by fever or signs of infection
  • causing confusion or severe exhaustion
  • significantly different from your usual symptoms

Even if previous episodes have been related to breathing pattern dysfunction, new or worsening symptoms should still be medically assessed.

Further Support

You may also find these resources helpful:

Last reviewed: May 2026
Produced by: National Aspergillosis Centre CARES Team / Aspergillosis Website

by GAtherton

Infographic showing causes of weight loss and weakness in aspergillosis including inflammation, reduced appetite, medication effects and muscle loss, with stages of recovery.

Weight Loss and Weakness in Aspergillosis: Why It Happens, How It Feels, and What Helps Recovery

Infographic showing causes of weight loss and weakness in aspergillosis including inflammation, reduced appetite, medication effects and muscle loss, with stages of recovery.
Weight loss and weakness in aspergillosis are usually caused by a combination of inflammation, increased energy use, reduced appetite, and muscle loss. Recovery is often gradual and happens in stages.

Last reviewed: April 2026

Unexpected weight loss and severe weakness are among the most worrying symptoms people report after being diagnosed with aspergillosis. Many describe feeling unlike themselves—physically drained, thinner than they have ever been, and struggling with everyday activities.

This article explains why this happens, what is going on in the body, and what recovery typically looks like.

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Key Points

  • Weight loss and fatigue are common in aspergillosis, particularly early in the illness or during flare-ups.
  • They are usually caused by a combination of inflammation, increased energy use, reduced appetite, and muscle loss.
  • Medication side effects can contribute but are rarely the main cause.
  • Many people improve over time, but recovery is usually gradual and can take weeks to months.
  • Stabilising weight is often the first important step before regaining strength.

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Contents

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Why does aspergillosis cause weight loss?

Weight loss in aspergillosis is rarely due to a single cause. Instead, it is usually the result of several overlapping processes.

1. Increased energy use (hypermetabolism)

When the body is dealing with infection or inflammation, it requires more energy. This is sometimes described as a hypermetabolic state.

  • The immune system is active and consumes energy
  • The body produces inflammatory signals
  • Breathing effort may increase

This means you may be burning more calories than usual—even at rest.

2. Reduced appetite

Many people notice they are eating less, sometimes without realising it. This may be due to:

  • Feeling unwell or fatigued
  • Shortness of breath when eating
  • Changes in appetite driven by inflammation

3. Medication effects

Some treatments can affect appetite or digestion. For example:

  • Antifungal medications such as itraconazole or voriconazole may cause nausea or taste changes
  • Steroids may increase appetite but can also contribute to muscle weakness over time

Medication effects vary widely and are usually only part of the overall picture.

4. Muscle breakdown

During illness, the body may break down muscle to meet energy needs. This can happen quickly, especially if activity levels fall.

This leads to:

  • Loss of strength
  • Reduced stamina
  • A feeling of being “weak” rather than just lighter

5. Underlying lung disease

Many people with aspergillosis also have conditions such as bronchiectasis, asthma, or chronic obstructive pulmonary disease (COPD). These can increase the effort required for breathing and contribute to ongoing energy use.

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What is happening inside the body?

Several biological processes contribute to weight loss and fatigue:

  • Inflammatory signalling: The immune system releases chemical signals that affect metabolism and appetite
  • Catabolism: The body breaks down tissues (including muscle) to release energy
  • Energy imbalance: More energy is used than consumed

This combination can make weight loss feel rapid and difficult to control.

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Which types of aspergillosis are affected?

These symptoms are most commonly seen in:

However, not everyone experiences weight loss, and severity varies.

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Why does it feel so severe?

Many people describe this stage as one of the most difficult parts of their illness. This is because several factors are happening at once:

  • Physical energy is reduced
  • Muscle strength has declined
  • The body is under ongoing stress
  • Recovery has not yet begun

This can make everyday activities—such as walking, cooking, or even eating—feel unusually difficult.

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Does it get better?

In many cases, yes—there is gradual improvement over time, especially once treatment begins to control the condition.

Recovery often follows a pattern:

  • Initial phase: weight loss and severe fatigue
  • Stabilisation: weight loss slows or stops
  • Recovery: gradual return of strength and energy

This process is usually slow and uneven, with good and bad days.

---

What can help day to day?

1. Focus on maintaining nutrition

  • Eat small amounts regularly rather than large meals
  • Choose foods that are easy to prepare and eat
  • Include protein to support muscle maintenance

2. Pace activity carefully

  • Gentle movement can help maintain strength
  • Avoid pushing too hard, as this can worsen fatigue
  • Increase activity gradually as energy improves

3. Look at trends over time

It can be helpful to focus on gradual changes such as:

  • Weight stabilising
  • Small improvements in energy

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Nutrition and rebuilding strength

Recovery often happens in stages:

  • Stage 1: Stabilising weight
  • Stage 2: Gradually increasing intake
  • Stage 3: Rebuilding muscle and strength

Regaining muscle mass takes time and usually follows once the underlying condition is better controlled.

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When to seek medical advice

You should contact your healthcare team if you experience:

  • Continued or rapid weight loss
  • Increasing weakness
  • Difficulty eating or swallowing
  • New or worsening symptoms

This may indicate the need for additional support or adjustment of treatment.

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Common questions

Is weight loss just due to poor appetite?

No. Reduced appetite is only one factor. Increased energy use and muscle loss are also important contributors.

Are medications the main cause?

Medications can contribute, but they are rarely the main reason for weight loss.

Will I regain my strength?

Many people do regain strength over time, although recovery is usually gradual.

Why does recovery take so long?

The body needs time to reduce inflammation, restore energy balance, and rebuild muscle.

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Summary

Weight loss and weakness in aspergillosis are common and can feel severe, particularly early in the illness. They are usually caused by a combination of increased energy use, reduced appetite, muscle loss, and underlying lung disease.

Although recovery can take time, many people improve gradually as treatment takes effect.

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Further Reading

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Author & Review

Prepared for aspergillosis.org to support patient understanding. Content reflects current clinical knowledge and patient-reported experience.

Disclaimer

This page is for general information only and does not replace advice from your healthcare team.

by GAtherton

Diagram showing why aspergillosis is often controlled rather than cured, including differences between ABPA and chronic pulmonary aspergillosis (CPA)

Can Aspergillosis Be Cured? Understanding Treatment, Control, and Long-Term Therapy

Last reviewed: April 2026

Key points

  • Aspergillosis is caused by fungi from the Aspergillus group.
  • Most people breathe in Aspergillus spores regularly without becoming ill.
  • In some people, damaged airways, lung cavities, mucus plugs, or immune responses allow the fungus or fungal material to persist.
  • Antifungal treatment may aim to cure, but in many cases the goal is long-term control.
  • Steroids can reduce harmful inflammation in allergic disease, but they can also reduce the body’s ability to clear fungus.

Table of contents

Overview

It is very common for people diagnosed with aspergillosis to feel worried when they read that others have been taking antifungal medication for months or even years.

This can lead to an understandable question:

“Does treatment actually work, or will I have this forever?”

The answer is more nuanced than a simple yes or no. Different forms of aspergillosis behave differently, and treatment goals vary depending on the condition.

Two of the most common conditions are:

Understanding this difference is key to understanding why treatment may continue for a long time.

If you would like a more detailed explanation of how these conditions are diagnosed and managed, see our guides to chronic pulmonary aspergillosis (CPA) and allergic bronchopulmonary aspergillosis (ABPA).

Why breathing in spores does not usually cause disease

Aspergillus spores are present in the environment, including air, soil, compost, dust, and decaying vegetation. Most people breathe in small numbers of these spores regularly without becoming ill.

In healthy lungs, spores are usually cleared by the immune system and by the normal cleaning mechanisms of the airways.

This means:

  • Exposure to Aspergillus is common
  • Most exposure does not lead to disease
  • Aspergillosis usually develops only when there are additional risk factors, such as lung damage, mucus trapping, or altered immune responses

So it is not accurate to think of most patients as being “constantly reinfected”. A better way to think about it is that some lungs provide conditions where Aspergillus, or fungal material, can persist and continue to cause problems.

Why aspergillosis can be hard to clear

Aspergillosis can be difficult to clear for several reasons. These include the structure of the lungs, the biology of the fungus, limitations of drug penetration, and the way the immune system responds.

1. Damaged lung tissue can provide protected spaces

In CPA, Aspergillus often grows in areas of abnormal lung, such as cavities, scarred tissue, or areas affected by bronchiectasis.

These areas can act as protected spaces where the fungus is harder for the immune system and antifungal medicines to reach.

2. Thick mucus can trap fungus and fungal material

In airway diseases such as asthma, bronchiectasis, and ABPA, thick mucus can trap spores, hyphae, and fungal fragments.

This trapped material can continue to stimulate inflammation even when the fungus is not invading lung tissue.

3. Antifungal medicines may suppress rather than sterilise

Antifungal medications can reduce fungal activity and help prevent progression, but they may not always remove every trace of fungus from damaged lung spaces or mucus-filled airways.

For this reason, success is often measured by:

  • Improved symptoms
  • Stabilised weight and energy
  • Fewer flare-ups
  • Stable or improved scans
  • Prevention of further lung damage

Infection and ABPA: different reasons for persistence

Chronic pulmonary aspergillosis: persistence of infection

In chronic pulmonary aspergillosis, the problem is fungal growth in damaged lung tissue.

  • Lung cavities provide spaces where fungus can grow
  • Drug penetration may be limited
  • The immune system may not fully clear infection

Allergic bronchopulmonary aspergillosis: persistence of reaction

In ABPA, the main issue is an exaggerated immune response.

  • Mucus traps fungal material
  • Small amounts can trigger strong reactions
  • Inflammation leads to more mucus

Do steroids influence this?

Yes. Steroids can be helpful but must be used carefully.

In ABPA, they reduce inflammation but may also reduce fungal clearance.

In chronic infection, steroids can increase the risk of persistence or progression.

Monitoring and drug interactions are important during treatment.

Control vs cure: what is the goal?

For many people, the realistic goal is:

  • Stability rather than eradication
  • Reduced symptoms
  • Prevention of progression

 

Diagram showing why aspergillosis is often controlled rather than cured, including differences between ABPA and chronic pulmonary aspergillosis (CPA)
Aspergillosis is often managed as a long-term condition. This diagram shows why complete cure can be difficult and how treatment focuses on control.

Common antifungal treatments

  • Itraconazole
  • Voriconazole
  • Posaconazole

These treatments are selected based on individual factors and require monitoring.

Why don’t I hear many success stories?

People who improve often post less, while those still struggling are more visible in forums.

When to seek medical advice

  • Uncertainty about treatment
  • Side effects
  • Weight loss
  • Worsening symptoms

Common questions

Can aspergillosis be cured?

Sometimes, but often it is managed long-term.

Are people constantly reinfected?

No. Most people clear spores regularly without issue.

Why is ABPA difficult to treat?

Because of ongoing immune reactions and mucus trapping.

Further reading

by GAtherton

Infographic showing ABPA cycle: Aspergillus spores, airway colonisation, immune reaction, inflammation and treatments including steroids and antifungals

ABPA: Allergic Reaction or Fungal Presence in the Lungs?

Infographic showing ABPA cycle: Aspergillus spores, airway colonisation, immune reaction, inflammation and treatments including steroids and antifungals
ABPA involves both an allergic response and the presence of Aspergillus in the airways, which can drive ongoing inflammation.

Allergic Bronchopulmonary Aspergillosis (ABPA) can be confusing. It is often described as an allergic condition, yet patients may also be told there is “fungus in the lungs”.

In reality, both can be true at the same time.

Key points

  • ABPA is primarily an allergic (immune) reaction to Aspergillus
  • The fungus can also persist in the airways (colonisation)
  • Colonisation is not the same as invasive infection
  • Steroids are the standard first-line treatment
  • Antifungals and biologics may be used in selected cases

What is ABPA?

ABPA is a condition where the immune system overreacts to a common environmental fungus, most often Aspergillus fumigatus.

For a full introduction, see our guide to
what is ABPA.

This leads to:

  • airway inflammation
  • increased mucus production
  • worsening asthma symptoms
  • raised Immunoglobulin E (IgE) levels

If you are unfamiliar with IgE, see
our explanation of IgE.

Importantly, ABPA is not an invasive fungal infection. The lungs are reacting to fungal material rather than being invaded by it.

Can the fungus live in the lungs?

Yes—this is an important nuance.

In people with conditions such as:

the structure of the airways can allow Aspergillus to persist in mucus within the airways. This is known as colonisation.

Colonisation means:

  • the fungus is present in airway mucus
  • it may grow at low levels locally
  • it does not invade lung tissue

This is very different from serious invasive fungal infections seen in severely immunocompromised patients.

How ABPA and colonisation interact

ABPA and colonisation are best understood as part of a spectrum of Aspergillus-related lung disease.

They can interact in a cycle:

  1. Aspergillus spores are inhaled
  2. The fungus persists in airway mucus
  3. The immune system reacts strongly (ABPA)
  4. Inflammation leads to more mucus production
  5. This creates an environment where the fungus can persist

This cycle can contribute to:

  • recurrent flare-ups
  • ongoing inflammation
  • persistently raised IgE levels

Standard treatment: steroids

Oral corticosteroids are the traditional first-line treatment for ABPA.

Steroids such as prednisolone are used because they:

  • reduce airway inflammation
  • suppress the allergic immune response
  • improve symptoms such as breathlessness and cough
  • help control flare-ups

Learn more in our guide to
steroids and aspergillosis.

Where do antifungals fit in?

Antifungal medications such as itraconazole are often used as an additional (adjunctive) treatment rather than the primary therapy.

The aim is to:

  • reduce the amount of fungus present in the airways
  • lower the trigger for the immune response
  • sometimes allow a reduction in steroid dose

For more detail, see our
antifungal treatments guide.

Biologic treatments

Biologic therapies such as omalizumab (anti-IgE) are increasingly used in some patients, particularly when:

  • symptoms are difficult to control
  • steroid side effects are significant
  • there is severe asthma alongside ABPA

Read more about
biologics in asthma and ABPA.

Why results and symptoms may not match

Some people with ABPA may feel relatively well but still have:

  • raised IgE levels
  • evidence of fungal presence in the airways

This is because blood tests reflect underlying immune activity, which does not always match how a person feels day to day.

Why treatment is individualised

Although steroids are the standard treatment, management is often tailored to the individual. This is because people may also have:

  • asthma
  • bronchiectasis
  • difficulty tolerating antifungal medications
  • side effects from long-term steroid use

Specialist teams balance these factors when planning treatment.

When to seek medical advice

People with ABPA should seek medical review if they experience:

  • worsening breathlessness
  • increased cough or sputum
  • new or persistent chest symptoms
  • possible medication side effects

Treatment decisions should always be made with a clinician experienced in managing Aspergillus-related lung disease.

Summary

  • ABPA is primarily an allergic condition
  • The fungus can also persist in the airways (colonisation)
  • These processes can drive each other
  • Steroids are the standard first-line treatment
  • Antifungals and biologics may be used in selected cases

Last reviewed: April 2026
Prepared by: National Aspergillosis Centre (patient information resource)

by GAtherton

Cystic Fibrosis, CFTR Gene Variants, and Aspergillosis

Last reviewed: 8 April 2026

Some people with aspergillosis are told they have cystic fibrosis (CF), or that they carry a CFTR gene variant. This can be unexpected and may raise concerns about whether this explains their symptoms or diagnosis.

This article explains how cystic fibrosis and CFTR gene variants relate to Aspergillus-related lung disease, what current research shows, and—importantly—what conclusions should not be drawn.

Contents

Key points

  • Most people with aspergillosis do not have cystic fibrosis.
  • Most people with cystic fibrosis do not develop ABPA or CPA.
  • ABPA is linked to mucus and immune responses, not just infection.
  • CFTR variants may contribute to risk in some people, but are usually only one factor.
  • CPA is mainly driven by structural lung damage, not CFTR genetics.

Back to top ↑

Important reassurance

Most people with aspergillosis do not have cystic fibrosis, and most people with cystic fibrosis do not develop Aspergillus-related disease.

Although these conditions can overlap, they are usually separate. Genetic findings such as CFTR variants should be interpreted carefully and in context.

Back to top ↑

What is cystic fibrosis?

Cystic fibrosis is a genetic condition caused by changes in the CFTR gene. This gene regulates salt and water movement across cells.

When CFTR function is reduced:

  • mucus becomes thick and sticky
  • airways are harder to clear
  • microorganisms persist more easily

This creates an environment where bacteria and fungi can accumulate over time.

Back to top ↑

What is a CFTR gene variant?

CFTR variants range from severe mutations (causing cystic fibrosis) to mild or uncertain variants.

Carriers (with one variant):

  • are common in the general population
  • usually have no symptoms
  • may have subtle effects in some cases

These subtle effects may include reduced mucus clearance or increased susceptibility to airway inflammation.

Back to top ↑

How CFTR affects the lungs

CFTR dysfunction affects the lungs in several key ways:

  • Mucus dehydration: mucus becomes thick and difficult to clear
  • Impaired clearance: particles and microbes remain in the airways
  • Chronic inflammation: immune responses become exaggerated

This combination creates a “retention environment” where inhaled organisms—including Aspergillus—may persist.

Back to top ↑

How Aspergillus behaves in the lungs

Aspergillus is inhaled by everyone, but its effects vary depending on the lung environment.

  • Healthy lungs: spores are cleared
  • Impaired clearance: spores may persist
  • Sensitive immune system: allergic reactions may develop
  • Damaged lungs: chronic infection may develop

This explains why Aspergillus-related disease is diverse and depends heavily on underlying lung conditions.

Back to top ↑

ABPA and cystic fibrosis

ABPA is an allergic immune reaction to Aspergillus.

It is recognised in cystic fibrosis because:

  • mucus retention increases exposure to Aspergillus
  • immune responses can be exaggerated

However:

  • Many CF patients never develop ABPA
  • Most ABPA patients do not have CF

Some studies suggest CFTR variants may increase susceptibility, but this is not consistent across all research.

Key message: ABPA and CF can overlap, but one does not imply the other.

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CPA and cystic fibrosis

CPA is a chronic fungal infection that develops in structurally damaged lungs.

The most important risk factor is:

pre-existing lung damage

This includes:

  • bronchiectasis
  • previous tuberculosis
  • COPD

Cystic fibrosis can lead to bronchiectasis, and therefore indirectly increase CPA risk.

However:

  • CPA is rarely driven directly by CFTR genetics
  • most CPA patients do not have CF

Key message: CPA is primarily a disease of lung structure, not genetics.

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Modern CF treatments and Aspergillus

CFTR modulators (such as elexacaftor/tezacaftor/ivacaftor) have transformed CF care.

They:

  • improve CFTR function
  • thin mucus
  • improve clearance

Studies suggest:

  • reduced Aspergillus detection in some patients
  • fewer ABPA exacerbations in some cases

However:

  • ABPA still occurs
  • existing lung damage remains
  • immune responses are not fully corrected

Overall: these therapies improve risk but do not eliminate Aspergillus-related disease.

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Does a CFTR variant explain symptoms?

No single factor explains complex lung disease.

Symptoms may result from:

  • underlying lung disease
  • infection
  • inflammation
  • environmental exposure

A CFTR variant may contribute, but is rarely the sole cause.

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What should patients take from this?

  • CF and CFTR variants can sometimes contribute
  • ABPA has the strongest connection
  • CPA is mainly driven by lung damage
  • Most patients with aspergillosis do not have CF

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When to seek medical advice

Seek advice if symptoms worsen, change, or include coughing up blood, fever, or chest pain.

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Conclusion

Cystic fibrosis and CFTR gene variants can play a role in some patients with Aspergillus-related lung disease, particularly where mucus clearance is affected. However, they should not be overemphasised. In most cases, they are just one part of a broader clinical picture involving lung structure, immune response, and environmental exposure.

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References

This article is for general information and does not replace advice from your clinical team.

by GAtherton