🧬 Could Antibody-Driven Dissolving of Charcot–Leyden Crystals Help ABPA?

Researchers have recently discovered that Charcot–Leyden crystals (CLCs) — the needle-shaped structures formed from the eosinophil protein galectin-10 — are not just debris.

In laboratory studies, specially designed antibodies can dissolve these crystals.

This has raised two important questions:

  1. Could dissolving the crystals reduce airway inflammation?

  2. Could dissolving them make mucus plugs easier to clear?

Here is what we currently know.

1️⃣ Could dissolving crystals reduce airway inflammation?

What we know

Laboratory and animal studies have shown:

  • Charcot–Leyden crystals can activate immune cells (especially macrophages).

  • They can stimulate inflammatory pathways (including inflammasome signalling).

  • In mouse models, antibodies targeting galectin-10 dissolved the crystals.

  • When crystals were dissolved, airway inflammation decreased.

This suggests that the crystals themselves may amplify inflammation, rather than simply mark it.

What this means biologically

In ABPA and eosinophilic asthma:

  • Eosinophils release galectin-10.

  • Galectin-10 crystallises.

  • Crystals may trigger further immune activation.

  • That leads to more inflammation → more eosinophils → more crystals.

Dissolving the crystals could theoretically interrupt this feedback loop.

How likely is this to help inflammation in humans?

Moderately plausible, but not yet proven.

The biological mechanism is strong.
The animal data are encouraging.
But no human clinical trials have yet shown reduced inflammation through crystal dissolution.

If developed successfully, this approach could:

  • Reduce airway immune activation

  • Lower exacerbation risk

  • Potentially reduce steroid dependence

But at present, it remains investigational.

2️⃣ Could dissolving crystals make mucus plugs easier to cough up?

This is more speculative — but still biologically reasonable.

Why mucus plugs are so thick in ABPA

ABPA mucus plugs contain:

  • Gel-forming mucins

  • DNA from inflammatory cells

  • Dead cells

  • Fungal fragments

  • Eosinophil proteins

  • Charcot–Leyden crystals

The crystals are:

  • Rigid

  • Needle-shaped

  • Structurally stable

When embedded in mucus, they likely increase:

  • Mechanical stiffness

  • Plug density

  • Resistance to deformation

From a physics perspective:

Removing rigid crystalline structures from a gel should reduce stiffness and improve flow.

Do we have direct evidence?

No.

There are currently:

  • No human studies measuring mucus clearance after crystal dissolution

  • No trials showing improved plug expectoration from crystal-targeting therapy

So while it is plausible that dissolving crystals could soften plugs, this has not yet been demonstrated in patients.

3️⃣ How strong is the overall case?

Outcome Evidence strength Likelihood
Reduced inflammation Strong biological rationale + animal data Moderately promising
Easier mucus clearance Biophysical plausibility only Possible but unproven

Inflammation reduction is the more evidence-supported target.
Improved plug clearance is plausible but currently theoretical.

4️⃣ How does this compare to existing treatments?

Current therapies (e.g., anti-IL-5 biologics) reduce eosinophils upstream.

That leads to:

  • Less galectin-10 release

  • Fewer crystals forming

  • Reduced inflammation

  • Often improved mucus plugging

So biologics already indirectly reduce crystal burden.

A crystal-dissolving antibody would act downstream, targeting the structural product directly.

This could theoretically:

  • Accelerate resolution of existing plugs

  • Reduce residual inflammatory signalling

But again, this remains in early research stages.

5️⃣ Practical take-home message

At present:

  • Dissolving Charcot–Leyden crystals reduces inflammation in animal models.

  • It is biologically plausible that this could also soften mucus plugs.

  • There is no human clinical proof yet.

  • No approved therapy currently targets the crystals directly.

The concept is scientifically credible — but still under development.

🔭 The Bigger Picture

ABPA is increasingly understood as a condition driven by:

  • Eosinophils

  • Allergic immune signalling

  • Abnormal mucus biology

  • Structural plug formation

Crystal-targeting therapies may eventually become part of a more precise approach to treating eosinophilic airway disease.

But for now, they remain a promising research direction rather than a clinical option.

by GAtherton

Systemic fungal infections: why speed, diagnosis and stewardship matter

Systemic fungal infections — including aspergillosis, candidiasis, cryptococcosis, mucormycosis and pneumocystis pneumonia — are medical emergencies. When diagnosis or treatment is delayed, mortality rises sharply. This comprehensive review brings together current understanding of how these infections arise, why they are so difficult to diagnose, and what is needed to improve outcomes.

Why fungal infections are often missed

Unlike many bacterial infections, systemic fungal infections can be hard to confirm quickly. Fungal organisms are often present in low numbers, may be released intermittently into the bloodstream, and can be difficult to grow in standard cultures. As a result, no single test is usually sufficient, and clinicians often need a combination of imaging, cultures, antigen tests, molecular tests (PCR), and histopathology.

Because delay can be fatal, antifungal treatment is frequently started on clinical suspicion alone — especially in critically ill or immunocompromised patients. The paper emphasises that this approach is often necessary, but it must be paired with a clear diagnostic strategy.

Antifungal stewardship: knowing when to stop

A central message of the paper is that diagnostic tests are just as important for stopping treatment as for starting it. Antifungal drugs can be toxic, interact with many other medicines, and drive antifungal resistance if used unnecessarily.

The authors stress that:

  • Diagnostic results should be actively reviewed

  • Antifungal therapy should be stopped or stepped down if infection is not supported by evidence

  • This approach protects patients and preserves antifungal effectiveness

Antifungal resistance is a growing threat

Antifungal resistance is no longer rare. The review highlights:

  • Azole resistance in Aspergillus, including cryptic species

  • Rising resistance in several Candida species

  • The global spread of multidrug-resistant Candida auris

Because of this, the authors recommend that all clinically relevant fungal isolates are identified to species level and tested for antifungal susceptibility wherever possible. Making assumptions about drug sensitivity is increasingly unsafe.

Aspergillosis: a broad spectrum of disease

The paper clearly outlines the many forms of aspergillosis, ranging from:

  • Allergic disease (such as allergic bronchopulmonary aspergillosis)

  • Chronic pulmonary aspergillosis, often in people with underlying lung damage

  • Subacute and acute invasive disease, particularly in immunocompromised or critically ill patients

Importantly, the review notes that aspergillosis is not limited to severely immunocompromised people. Chronic and subacute forms often occur in individuals with structural lung disease who are otherwise immunocompetent.

Climate change and emerging fungal risks

One of the most forward-looking sections of the paper addresses how climate change and natural disasters are altering fungal disease patterns. Rising environmental temperatures, flooding, storms and environmental disruption are:

  • Increasing exposure to environmental fungi

  • Enabling fungi to adapt to higher temperatures

  • Contributing to outbreaks after natural disasters and trauma

  • Expanding fungal diseases into new geographic regions

The authors argue that fungal infections must be considered part of future public health and healthcare resilience planning.

Key take-home messages

  • Systemic fungal infections are time-critical medical emergencies

  • Diagnosis usually requires multiple tests, not a single result

  • Early antifungal treatment is often necessary — but must be reviewed

  • Diagnostics are essential for safe antifungal stewardship

  • Antifungal resistance is a real and growing problem

  • Climate change is reshaping fungal epidemiology and risk

Free access to the full article

Elsevier has provided free access to the full paper for a limited time (no registration required):

👉 https://authors.elsevier.com/a/1mZqR4qdNoJLH2
🗓️ Available until 28 March 2026

This article is recommended reading for patients wanting a deeper understanding of fungal disease, as well as clinicians, microbiology teams, and healthcare planners.

by GAtherton

Weekly Aspergillosis Update (2–9 February 2026)(Week 5).

This week’s papers cluster around: (1) ICU/viral-pneumonia–associated invasive pulmonary aspergillosis (IPA),
(2) tuberculosis (TB)–chronic pulmonary aspergillosis (CPA) overlap,
(3) diagnostic criteria and emerging detection approaches, and
(4) antifungal drug interaction risk.

Top highlights (quick take)

  • CAPA criteria matter: case rates vary substantially depending on which definition is used (AspICU vs ISHAM vs EORTC).
  • Viral illness + immune dysfunction = early IPA risk: data add to the “risk stacking” story (including SFTS and broader viral pneumonia).
  • TB–CPA remains a major clinical challenge: CPA can be misread as TB relapse; delayed recognition worsens outcomes.
  • Safety: rifapentine can markedly reduce voriconazole exposure (important in TB–aspergillosis co-infection).

1) ICU, Viral Pneumonia & CAPA / IPA


Decoding CAPA: A Comparative Study of Aspicu, Isham, and Eortc Criteria in Critical COVID-19 Patients Requiring Mechanical Ventilation (Preprint)

Taleb C, Lelubre C, Biston P, Piagnerelli M. Preprints.org. 04 Feb 2026. PPR: PPR1150994

  • What they did: compared CAPA classification using AspICU, ISHAM and EORTC-style criteria in ventilated COVID-19 patients.
  • Key point: CAPA “incidence” changes materially depending on the criteria applied; distributions differed across COVID-19 waves.
  • Why it matters: reinforces that audits, research comparisons and ICU protocols must state which definition is used (and why).


Characteristics of T-lymphocyte subsets in patients with severe fever with thrombocytopenia syndrome complicated with invasive pulmonary aspergillosis: a retrospective study

Xu Y, Liu Y, Qian Y, et al. Front Immunol. 09 Feb 2026. PMCID: PMC12876148

  • What they found: SFTS patients complicated by IPA showed marked T-cell subset abnormalities and high reported secondary IPA rates.
  • Clinical takeaway: another example of viral immune dysregulation predisposing to IPA—analogous to influenza-associated IPA and CAPA.
  • Practice relevance: supports heightened fungal vigilance in severe viral syndromes with immune suppression features.


Immunocompromise and early-onset invasive pulmonary aspergillosis in viral pneumonia: a retrospective cohort study

Sun B, Shen J, Dong M, et al. Front Public Health. 02 Feb 2026. PMCID: PMC12852324

  • Theme: early IPA can emerge in viral pneumonia in the setting of immunocompromise (not only classic neutropenia).
  • Why it matters: backs the “risk stacking” concept—viral lung injury + immune dysfunction (often steroids) can accelerate IPA risk.
  • Use: helpful citation for ICU pathways and education materials.


The COVID-19 pandemic: an underlying factor for increased Stenotrophomonas maltophilia infections—A literature review and case study analysis (Review)

Pompilio A, Di Bonaventura G. Front Microbiol. 06 Feb 2026. PMCID: PMC12867275

  • What’s relevant to aspergillosis: notes co-detection of Stenotrophomonas maltophilia in COVID-19 patients with invasive aspergillosis.
  • Why it matters: underlines polymicrobial complexity in ICU; prompts questions about dysbiosis and pathogen interactions in severe disease.


Pulmonary Cavitation as a Late and Self-Limited Complication of COVID-19 Pneumonia: A Case Report

Osório M, Silveira M. Cureus. 02 Feb 2026. PMCID: PMC12852039

  • Clinical reminder: post-COVID cavitation has a broad differential including CAPA and mucormycosis; requires careful exclusion of fungal disease.
  • Why it matters: useful for follow-up imaging discussions and MDT differential diagnosis teaching.

2) TB–CPA overlap & antifungal pharmacology


Clinical features, diagnostic test performance, treatment and outcome of pulmonary tuberculosis patients with chronic pulmonary aspergillosis in China: a retrospective, observational study

Li J, Wu N, Mei C, et al. Front Cell Infect Microbiol. 06 Feb 2026. PMCID: PMC12864492

  • Main message: CPA in TB patients is common and can be mistaken for TB relapse; diagnostic delay is consequential.
  • Why it matters: strong global relevance—TB remains one of the biggest drivers of CPA burden.
  • Use: good reference for post-TB lung disease pathways and CPA awareness materials.


A clinically significant interaction between voriconazole and rifapentine: a case report and review of evidence

Chen T, Chen X, Zhang Q. Front Med (Lausanne). 09 Feb 2026. PMCID: PMC12875967

  • What happened: TB–aspergillosis co-infection complicated by rifapentine–voriconazole interaction.
  • Key point: rifapentine (a potent enzyme inducer) can substantially reduce voriconazole exposure → risk of treatment failure.
  • Why it matters: high-impact safety message; supports use of therapeutic drug monitoring and/or alternative strategies in TB co-treatment.

3) Diagnostics & detection methods


Combined Biospectroscopy with Multivariate Analysis for the Differential Diagnosis of Leptospirosis Disease: A Pilot Study

Zambrano A, Trilleras J, Arana Rengifo V, et al. ACS Omega. 09 Feb 2026. PMCID: PMC12878783

  • Why it’s here: includes a small aspergillosis group among comparator infections.
  • What it suggests: biospectroscopy + multivariate modelling may separate infections via biochemical “fingerprints” (early-stage concept).
  • Bottom line: promising research direction, but not near-term clinical practice.


Research progress on the current status of respiratory pathogen infections and their detection methods (Review)

Zhu F, Peng M, Chen A, Zhu Q. Front Microbiol. 09 Feb 2026. PMCID: PMC12876234

  • Scope: broad overview of respiratory pathogen detection, including invasive and allergic aspergillosis concepts.
  • Useful for: background reading for non-specialists and training materials (diagnostic modalities and limitations).

4) Aspergillus biology, pathology & wider fungal immunology


Characterization of a bZIP Transcription Factor ZipD in Aspergillus flavus

Jeong D, Cho H, Park H. Mycobiology. 06 Feb 2026. PMCID: PMC12865826

  • What it is: basic science on gene regulation (ZipD) in Aspergillus flavus.
  • Why it matters: contributes to long-term understanding of fungal stress responses and potential future targets.


Mechanistic Insights into Calcium Oxalate Crystals in Aspergillosis of the Maxillary Sinus

Trimukhe A, Bhatt K, Mridha AR, et al. Head Neck Pathol. 02 Feb 2026. PMID: 41627592

  • Key message: calcium oxalate crystal deposition is a mechanistic contributor to local inflammation/tissue injury in sinus aspergillosis.
  • Clinical relevance: useful for ENT/pathology audiences; supports recognition of crystals as an important clue.


Adjunctive GM-CSF therapy enhances host defense against systemic Candida auris infection in immunosuppressed mice

Mattos E, Das Gupta K, Quintanilla D, et al. Front Immunol. 06 Feb 2026. PMCID: PMC12862068

  • Why included: host-directed immunotherapy concepts often discussed alongside invasive aspergillosis.
  • Takeaway: GM-CSF improved antifungal host defense in a preclinical model—supporting interest in adjunctive approaches (not clinical guidance).


The therapeutic potential of high-dose inhaled nitric oxide for antimicrobial effects: a narrative review and future directions (Review)

Berra L, Kamenshchikov N, Tal A, et al. Intensive Care Med Exp. 05 Feb 2026. PMCID: PMC12872992

  • Scope: experimental antimicrobial strategy, mainly ICU-focused.
  • Relevance: future-facing adjunct discussion rather than current aspergillosis practice.

5) Case reports & broader context (selected)


Case Report: Triple autoimmune overlap: rheumatoid arthritis, systemic lupus erythematosus, and hypereosinophilic asthma with systemic manifestations

Front Immunol. 02 Feb 2026. PMCID: PMC12852425

  • Aspergillosis relevance: ABPA considered in complex eosinophilic/asthma phenotypes; reminder that ABPA can present atypically (e.g., without classic bronchiectasis early on).
  • Use: supports education on diagnostic nuance in asthma/eosinophilic lung disease.


HIV-associated neurological infections in a Brazilian tertiary care center: clinical-epidemiological features and predictors of in-hospital mortality

Ramos L, Ninomiya D, Sequeira M, et al. Rev Inst Med Trop Sao Paulo. 02 Feb 2026. PMCID: PMC12858172

  • Context: opportunistic infection landscape in advanced HIV; useful epidemiological background (limited direct aspergillosis focus).

Note: This page summarises research and does not replace clinical guidance. If you are a patient and have concerns about symptoms or treatment, contact your clinical team.

by GAtherton

Can blood tests help predict if chronic pulmonary aspergillosis will come back?

This study from the National Aspergillosis Centre (NAC) looked at people with chronic pulmonary aspergillosis (CPA) who had completed antifungal treatment and asked a simple question:

Can blood tests tell us who is more likely to relapse after treatment stops?

What the researchers did

Doctors reviewed patients with CPA who had:

  • Taken antifungal treatment for at least 6 months

  • Stopped treatment because they were clinically stable

They then followed these patients to see who stayed well and who relapsed, and compared this with their blood test results at the time treatment stopped.

What they found

  • About 1 in 4 patients had a relapse after stopping treatment

  • People whose Aspergillus IgG blood test was still high at the end of treatment were much more likely to relapse

  • Patients whose IgG level had fallen to a lower level did not relapse in this study

  • Signs of Aspergillus allergy or sensitisation also increased relapse risk

  • CT scan appearances and treatment length alone were not reliable predictors

Why this matters for patients

This means that:

  • Blood tests may help doctors decide when it is safe to stop treatment

  • Some people may need closer follow-up or longer treatment

  • Follow-up can be more personalised, rather than “one size fits all”

Importantly, a relapse does not mean treatment failed — it reflects how persistent this infection can be in damaged lungs.

Key takeaway

A simple blood test at the end of treatment may help predict who needs closer monitoring for CPA relapse.

This research supports a more individualised approach to long-term CPA care.

by GAtherton

Aspergillosis, immunity, and risk

Primary immune deficiencies and immune modifiers explained

A single, comprehensive explainer for expert patients, carers, and non-specialists

Why this article exists

Aspergillus is a mould that everyone breathes in every day. Most people clear it without difficulty.
A small number of people develop aspergillosis because the balance between the fungus, the lungs, and the immune system is disturbed.

This article explains:

  • Rare primary (inherited) immune deficiencies that are clearly linked to aspergillosis

  • Common immune “modifier” factors that can increase risk or severity but do not cause disease on their own

  • How these factors stack together in real life

Key reassurance up front

  • There are 500+ recognised primary immune deficiencies

  • Only ~20–30 are clearly linked to aspergillosis

  • Most people with aspergillosis do not have any inherited immune disorder

The unifying concept: three immune pathways to aspergillosis

Almost all immune–aspergillus relationships fall into three mechanisms. Understanding these matters more than memorising names.

1. Reduced ability to kill the fungus

Some immune cells fail to destroy Aspergillus spores effectively.
→ Risk of invasive aspergillosis, sometimes severe or life-threatening.

2. Lung damage over time

Repeated infections or inflammation damage airways or leave cavities.
→ Risk of chronic pulmonary aspergillosis (CPA) or aspergillomas.

3. Excessive allergic inflammation

The immune system over-reacts to Aspergillus rather than failing to fight it.
→ Allergic bronchopulmonary aspergillosis (ABPA) and severe fungal-sensitised asthma.

Many conditions overlap more than one pathway.

Section 1: Primary (inherited) immune deficiencies clearly linked to aspergillosis

Rare, high-impact, and sometimes life-changing when present

These are the conditions clinicians usually mean when they talk about “immune causes of aspergillus disease”.

A. Phagocyte defects

Strongest association with invasive aspergillosis

  1. Chronic granulomatous disease (CGD)

  2. Autosomal recessive forms of CGD

  3. Severe congenital neutropenia

  4. Cyclic neutropenia

  5. Leukocyte adhesion deficiency type I

Typical pattern

  • Aspergillosis at a young age

  • Invasive lung disease ± spread beyond lungs

  • Often no other obvious risk factors

B. Hyper-IgE and severe allergy syndromes

Allergic, chronic, and cavity-associated disease

  1. STAT3 hyper-IgE syndrome

  2. DOCK8 deficiency

  3. PGM3 deficiency

  4. ZNF341 deficiency

  5. IL6ST deficiency

Typical pattern

  • Severe asthma and allergy

  • Thick mucus, recurrent infections

  • ABPA, later CPA or aspergillomas

C. Combined immunodeficiencies

Immune coordination problems

  1. Severe combined immunodeficiency (milder or surviving forms)

  2. Omenn syndrome

  3. ZAP-70 deficiency

  4. Major histocompatibility complex class II deficiency

  5. CD40 ligand deficiency (hyper-IgM syndrome)

Typical pattern

  • Broad infection susceptibility

  • Aspergillosis can behave aggressively

D. Defects of fungal recognition and innate signalling

Often dramatic or unexpected presentations

  1. CARD9 deficiency

  2. Dectin-1 (CLEC7A) complete deficiency

  3. MALT1 deficiency

Typical pattern

  • Severe or unusual aspergillosis

  • Lung, brain, or deep tissue involvement

  • Sometimes first presents in adulthood

E. Immune dysregulation syndromes

Mixed infection, inflammation, and autoimmunity

  1. CTLA-4 haploinsufficiency

  2. LRBA deficiency

  3. STAT1 gain-of-function mutations

  4. IPEX syndrome (FOXP3 deficiency)

Typical pattern

  • Inflammatory lung disease

  • Chronic or invasive aspergillosis emerging over time

F. Antibody deficiencies (indirect risk via lung damage)

  1. Common variable immunodeficiency

  2. X-linked agammaglobulinaemia

  3. Activated PI3K-delta syndrome

Important nuance
Antibodies do not normally kill Aspergillus.
Risk arises after years of lung damage, not early in life.

Section 2: Immune modifier-types that can amplify risk

Common, low-penetrance, and often invisible on routine testing

These are not immune deficiencies, but they can influence who struggles, how severely, and why disease persists.

Mannose-binding lectin (MBL) deficiency

  • Common (≈5–10% of population)

  • Affects fungal recognition and complement activation

  • Usually mild on its own

  • Becomes relevant with lung disease, steroids, or other immune issues

Partial fungal-recognition receptor variants

  • Heterozygous dectin-1 variants

  • Toll-like receptor polymorphisms (for example TLR2, TLR4)

Effect

  • Slower fungal recognition

  • Increased colonisation or allergic response

  • Act as risk amplifiers, not causes

Cytokine balance variants

Small genetic differences affecting immune “signal strength”, including:

  • Interleukin-6

  • Interleukin-10

  • Tumour necrosis factor-alpha

These modify:

  • Inflammation intensity

  • Tissue damage vs clearance balance

Allergy-biased (Th2-skewed) immunity

Not a disease, but a recognised immune tendency.

Features:

  • Asthma

  • Eczema

  • Nasal polyps

  • High immunoglobulin E levels

  • Eosinophilia

Strongly associated with:

  • Fungal sensitisation

  • ABPA

  • Difficult-to-control asthma

Impaired mucociliary clearance

A functional immune–mechanical issue.

Seen in:

  • Severe asthma

  • Bronchiectasis

  • Chronic sinus disease

Effect:

  • Aspergillus spores are not physically cleared

  • Prolonged immune exposure

  • Increased colonisation and allergy

Age-related immune change (immunosenescence)

  • Normal reduction in immune speed and coordination with age

  • Particularly relevant to chronic pulmonary aspergillosis

Not a disease, but an important modifier of outcome.

Airway epithelial vulnerability

Subtle weaknesses in:

  • Airway lining integrity

  • Antimicrobial peptide production

  • Local immune signalling

Can increase:

  • Fungal adherence

  • Chronic colonisation

  • Allergic sensitisation

Section 3: Risk stacking – how this works in real life

Aspergillosis rarely results from one single factor.

Instead, several modest risks align:

  • Mild MBL deficiency

  • Severe asthma

  • Corticosteroid exposure

  • Bronchiectasis

  • Age-related immune change

→ Together, they create real disease risk, even though none alone would.

This explains why:

  • Two people with similar scans can behave very differently

  • One patient relapses while another stabilises

  • “Why me?” often has no single answer

Section 4: When clinicians investigate immune causes

Testing is targeted, not routine. It is usually considered when there is:

  • Aspergillosis at a young age

  • Invasive or unusually severe disease

  • Disease without classic risk factors

  • Recurrent infections plus severe asthma or allergy

  • A family history of unusual infections

Section 5: Why identifying (or excluding) immune factors helps

Understanding immune contribution can:

  • Explain disease pattern and behaviour

  • Guide antifungal choice and duration

  • Inform long-term prevention strategies

  • Reduce future lung damage

  • Reassure patients when no immune defect is found

Key take-home messages

  • Aspergillus exposure is universal; immune causes are rare

  • Only ~20–30 inherited immune deficiencies are clearly linked to aspergillosis

  • Modifier-type immune factors are common and usually harmless alone

  • Aspergillosis often reflects risk stacking, not a single diagnosis

  • Understanding patterns matters more than labels

  • Specialist care improves precision and outcomes

by GAtherton

Latest Aspergillosis & Related Research Updates (Week 4).

Executive overview (what stands out this fortnight)

Key signals

  • Immune dysregulation—not just classic immunosuppression—continues to emerge as a central driver of invasive aspergillosis.

  • Allergic bronchopulmonary aspergillosis (Allergic Bronchopulmonary Aspergillosis) is appearing in atypical and early phenotypes, including absence of bronchiectasis.

  • Antifungal toxicity and pharmacokinetic variability remain clinically important.

  • Paediatric invasive aspergillosis evidence is improving.

  • Environmental and One Health studies continue to inform exposure risk.

  • Overlap with non-tuberculous mycobacteria and microbiome disruption is increasingly evident.

1. Immunocompromise, viral infection, and invasive aspergillosis
Immunocompromise and early-onset invasive pulmonary aspergillosis in viral pneumonia

Sun B et al., Frontiers in Public Health, 2026

Relevance

  • Directly informs understanding of early invasive pulmonary aspergillosis in severe viral pneumonia.
  • Extends COVID-associated pulmonary aspergillosis concepts to non-COVID viral infections.

Key points

  • Viral pneumonia causes early immune dysregulation, including lymphopenia.
  • Invasive aspergillosis may develop before classic intensive care risk factors.
  • Supports earlier fungal surveillance rather than late rescue testing.

Pulmonary cavitation as a late and self-limited complication of COVID-19 pneumonia

Osório M, Silveira M, Cureus, 2026

Relevance

  • Highlights post-viral structural lung damage as a substrate for aspergillosis.

Key points

  • Cavitation discussed alongside COVID-associated pulmonary aspergillosis and mucormycosis.
  • Fungal risk may persist after apparent clinical recovery.

2. Allergic disease and ABPA – expanding phenotypes
Triple autoimmune overlap: rheumatoid arthritis, systemic lupus erythematosus, and hypereosinophilic asthma with ABPA features

Frontiers in Immunology, 2026 (Case Report)

Relevance

  • Challenges rigid diagnostic frameworks for Allergic Bronchopulmonary Aspergillosis.
  • Supports emerging views that ABPA can occur before bronchiectasis develops.

Key points

  • ABPA considered despite normal chest imaging.
  • Diagnosis driven by immunological and eosinophilic markers.

Diagnosis of bronchopulmonary candidiasis—refractory airway hyperresponsiveness and severe pneumonia

Zhang D et al., Frontiers in Medicine, 2026

Relevance

  • Important differential diagnosis for suspected ABPA.

Key points

  • Bronchopulmonary candidiasis can closely mimic ABPA.
  • Normal Aspergillus serology does not exclude other fungal airway disease.

3. Rare immune defects and aspergillosis
Complete and partial forms of X-linked MCTS1 deficiency in patients with mycobacterial disease

Zhou Q et al., Journal of Human Immunity, 2026

Relevance

  • Expands the list of primary immunodeficiencies associated with Aspergillus infection.

Key points

  • Central nervous system aspergillosis identified as a rare but severe phenotype.
  • Suggests impaired cellular immunity as the underlying mechanism.

4. Antifungal therapy – toxicity, variability, and paediatrics
Voriconazole-associated peripheral polyneuropathy: A case report

González BJ et al., Archives of Argentine Pediatrics, 2026
(No PMC full text currently available)

Relevance

  • Highlights clinically important non-hepatic toxicity of azole therapy.

Key points

  • Peripheral neuropathy developed during voriconazole treatment.
  • Symptoms may be insidious and progressive.

RE: Factors affecting voriconazole pharmacokinetic variability in critically ill patients

Langbeen J et al., Critical Care, 2026

Relevance

  • Explains why fixed dosing of voriconazole is often unsafe.

Key points

  • Critical illness alters drug metabolism and clearance.
  • Drug–drug interactions are common.
  • Supports therapeutic drug monitoring and specialist pharmacy input.

Phase 2 clinical trial of posaconazole in paediatric invasive aspergillosis

Kang HJ et al., Antimicrobial Agents and Chemotherapy, 2026
(No PMC full text currently available)

Relevance

  • Rare prospective antifungal data in children.

Key points

  • Posaconazole showed acceptable safety.
  • Clinical responses were encouraging in a high-risk population.

5. Diagnostics, microbiology, and co-infection
Clinical characteristics, molecular diagnosis, and drug resistance profiles of nontuberculous mycobacteria infections

Wang K et al., Clinical and Translational Science, 2026

Relevance

  • Highly relevant to bronchiectasis patients where NTM and aspergillosis frequently coexist.

Key points

  • Molecular diagnostics improve species identification.
  • Resistance patterns complicate treatment strategies.

Impaired systemic antibody response against gut microbiota pathobionts in critical illness

Cho NA et al., Intensive Care Medicine Experimental, 2026

Relevance

  • Links immune–microbiome disruption to susceptibility to Aspergillus fumigatus.

Key points

  • Critical illness impairs antibody responses.
  • Loss of immune balance increases infection risk.

6. Pathogenesis and basic science
Arp2/3 complex contributes to actin-dependent uptake of Aspergillus terreus conidia

Mach N et al., PLOS One, 2026

Relevance

  • Improves understanding of early host–fungus interactions.

Key points

  • Epithelial cells actively internalise Aspergillus conidia.
  • Species differences may influence pathogenicity.

7. Environmental and One Health perspectives
Seasonal variation in Aspergillus abundance in captive penguin burrow sands

Takanobu S et al., Frontiers in Veterinary Science, 2026

Relevance

  • Demonstrates dynamic environmental exposure risk.

Key points

  • Clear seasonal peaks in Aspergillus burden.
  • Correlates with increased disease risk.

Mycotoxins – biomonitoring method including gliotoxin

Berger M et al., MAK Collection for Occupational Health and Safety, 2026

Relevance

  • Gliotoxin explored as a potential biomarker for invasive aspergillosis.

Key points

  • LC-MS/MS methods validated.
  • Currently research-grade rather than clinical.

by GAtherton

Latest Aspergillosis & Related Research Updates (Week 3).

January–February 2026

Search term is 'aspergillosis'.

This update highlights recent publications relevant to aspergillosis, allergic bronchopulmonary aspergillosis, nontuberculous mycobacterial lung disease, antifungal stewardship, diagnostics, and environmental fungal exposure. Papers are grouped by clinical theme, with key findings and clinical relevance highlighted.

1. Diagnostics, Molecular Methods & Imaging Innovation

Clinical Characteristics, Molecular Diagnosis, and Drug Resistance Profiles of Nontuberculous Mycobacteria Infections

Wang K, Xu D, Gao Y, Zhao W, Ma K
Clinical and Translational Science, 19(2):e70479, Feb 2026

Key highlights

  • Retrospective analysis using polymerase chain reaction melting curve technology to identify nontuberculous mycobacterial species.

  • Demonstrates rapid differentiation of clinically relevant species, with integrated resistance profiling.

  • Highlights marked heterogeneity in clinical presentation and antimicrobial resistance patterns.

Why this matters

  • Increasing relevance for patients with bronchiectasis, chronic obstructive pulmonary disease, and aspergillosis, where nontuberculous mycobacteria co-infection complicates diagnosis and treatment.

  • Supports the shift away from prolonged culture-only pathways toward faster molecular diagnostics.

Amplicon-based sequencing as a diagnostic tool for severe pneumonia in the ICU

Michel C, Imamura H, Yin N, et al.
Scientific Reports, 16(1):2845, Jan 2026

Key highlights

  • Amplicon-based sequencing applied directly to respiratory samples in intensive care.

  • Detects invasive aspergillosis alongside bacterial and viral pathogens.

  • Highlights limitations of current definitions of “proven invasive aspergillosis” when relying solely on histopathology.

Why this matters

  • Reinforces the diagnostic gap in critical care–associated pulmonary aspergillosis.

  • Supports broader adoption of molecular and microbiome-informed diagnostics in high-risk settings.

Deep learning detection and classification of fungal and non-fungal calcifications on paranasal sinus CT imaging

Yang Z, Choi I, Yun H, et al.
PLOS One, 21(1):e0340832, Jan 2026

Key highlights

  • Deep learning model distinguishes fungal ball (commonly aspergillosis) from non-fungal calcifications.

  • High diagnostic accuracy on routine sinus computed tomography scans.

  • Addresses a frequent diagnostic uncertainty in chronic rhinosinusitis.

Why this matters

  • Potential to reduce diagnostic delay and unnecessary surgery.

  • Particularly relevant for centres without ready access to specialist radiology expertise.

2. Invasive Aspergillosis: Expanding Risk Profiles & Clinical Phenotypes

Unmasking Invasive Pulmonary Aspergillosis: Insights From a Case Series at a Tertiary Care Center

Munasinghe K, Nanayakkara A, De Zoysa W, et al.
Cureus, 17(12), Jan 2026

Key highlights

  • Case series illustrating heterogeneous clinical presentations.

  • Emphasises delayed recognition outside classic immunocompromised populations.

  • Reinforces global incidence estimates of approximately 250,000 cases annually.

Why this matters

  • Supports growing recognition that invasive pulmonary aspergillosis occurs in broader patient groups, including those with chronic lung disease and critical illness.

Disseminated Invasive Aspergillosis in a Young Patient With Chronic Alcohol Use and Seemingly Preserved Immunocompetence

Khandwala K, Sawliha Syed H, Anwar S, et al.
Clinical Case Reports, 14(2), Jan 2026

Key highlights

  • Disseminated disease involving multiple organs.

  • Chronic alcohol use identified as a functional immunosuppressive state.

  • Challenges traditional “immunocompetent vs immunocompromised” dichotomy.

Why this matters

  • Reinforces the need for high clinical suspicion even when standard immune markers appear preserved.

  • Relevant for emergency, acute medical, and respiratory teams.

Intensification of Treosulfan–Fludarabine Conditioning With Thiotepa in Allogeneic Hematopoietic Stem Cell Transplantation

Tosoni L, Facchin G, Plos R, et al.
Transplant Direct, 12(2):e1896, Jan 2026

Key highlights

  • Real-world study in older or comorbid transplant recipients.

  • Reports four cases of invasive aspergillosis (three pulmonary, one cerebral).

  • Conditioning regimen was otherwise effective and tolerable.

Why this matters

  • Reinforces persistent invasive fungal infection risk despite modern conditioning approaches.

  • Supports ongoing need for antifungal prophylaxis and surveillance.

Infective Endocarditis Caused by Pan-Azole-Resistant Aspergillus fumigatus in a Lung Transplant Recipient

Ukai K, Kawashima M, Ikeuchi K
Transplant Infectious Disease, Jan 2026

Key highlights

  • Rare but severe manifestation: fungal endocarditis.

  • Pan-azole resistance significantly limited treatment options.

  • Occurred in a lung transplant recipient.

Why this matters

  • Adds to evidence of clinically catastrophic azole resistance.

  • Reinforces importance of resistance testing and antifungal stewardship.

3. Antifungal Toxicity & Stewardship

Voriconazole-associated peripheral polyneuropathy: A case report

González BJ, Ivarola P, Miranda M, et al.
Archivos Argentinos de Pediatría, 124(1), Feb 2026

Key highlights

  • Documents peripheral neuropathy linked to prolonged voriconazole exposure.

  • Emphasises reversibility only after early recognition and drug withdrawal.

Why this matters

  • Highly relevant for patients on long-term antifungal therapy for chronic pulmonary aspergillosis.

  • Supports routine neurological symptom surveillance.

Antifungal Stewardship: Time to Reappraise the Priorities toward Increasing Invasive Fungal Infections

Singh S
Annals of African Medicine, Jan 2026

Key highlights

  • Reviews stewardship challenges across aspergillosis, candidemia, and mucormycosis.

  • Highlights overuse, under-diagnosis, and limited access to diagnostics.

  • Calls for stewardship frameworks equivalent to antibacterial programmes.

Why this matters

  • Directly relevant to azole resistance, drug toxicity, and resource-limited settings.

  • Aligns with national and international fungal disease priorities.

4. Allergy, Mycotoxins & Inflammatory Pathways

Common inflammatory markers predict risk of ABPA development in children with cystic fibrosis

Crabtree HED, Malajczuk CJ, Ho HY, et al.
Journal of Cystic Fibrosis, Jan 2026

Key highlights

  • Identifies routinely measured inflammatory markers predictive of allergic bronchopulmonary aspergillosis.

  • Potential for earlier identification and intervention.

Why this matters

  • May support risk stratification in paediatric cystic fibrosis clinics.

  • Relevant for future screening and monitoring protocols.

Potential mechanisms and effects of AFB1-induced asthma

Yu Z, Gao M, Wu X, et al.
PLOS One, 21(1):e0341172, Jan 2026

Key highlights

  • Network toxicology and molecular docking suggest links between aflatoxin B1 exposure and:

    • Asthma

    • Allergic bronchial pulmonary aspergillosis

    • Lung malignancy in severe cases

Why this matters

  • Strengthens environmental and occupational health links to fungal allergy and chronic lung disease.

  • Supports broader discussion of mould exposure beyond infection alone.

Mycotoxins – Determination of aflatoxins, ochratoxin A, gliotoxin, and others in urine by LC–MS/MS

Berger M, Deharde M, Neuhoff J, et al.
MAK Collection for Occupational Health and Safety, 10(2), Jan 2026

Key highlights

  • Validated biomonitoring method for gliotoxin, aflatoxins, and ochratoxins.

  • Discusses potential use of urine biomarkers for early detection of invasive aspergillosis.

Why this matters

  • Provides methodological groundwork for future biomarker-driven diagnostics.

  • Particularly relevant for occupational and environmental exposure assessment.

Money and Microbes: A Global Systematic Review and Meta-Analysis of Currency Contamination

Appiah PO, Odoom A, Tetteh-Quarcoo PB, Donkor ES
Environmental Health Insights, Jan 2026

Key highlights

  • Identifies paper currency as a reservoir for microbial and fungal contamination.

  • Notes links to serious infections, including pulmonary aspergillosis.

Why this matters

  • Highlights overlooked environmental reservoirs of fungal exposure.

  • Relevant for public health messaging and infection control.

by GAtherton

Connecting patients, carers, clinicians and scientists to improve life with aspergillosis

World Aspergillosis Day (WAD) is an annual global event that brings together people who live with, care for, treat, and research long-term forms of aspergillosis — particularly chronic pulmonary aspergillosis (CPA) and allergic bronchopulmonary aspergillosis (ABPA).

Each year, WAD creates a shared space where:

  • patients and carers can hear directly from specialists,

  • clinicians and scientists can learn from patient experience,

  • and everyone can explore how new research translates into better care.

🎥 Missed previous events?
Recordings from earlier World Aspergillosis Day meetings are available on our YouTube channel.

📅 NAC World Aspergillosis Day Meeting 2026

The National Aspergillosis Centre (NAC) will once again host a free online meeting:

🗓 Tuesday 3 February 2026
💻 Online via Microsoft Teams
👥 Open to patients, carers, clinicians, scientists, and anyone who lives or works with aspergillosis

🧬 This year’s theme:

“How can the genomics revolution help patients with chronic aspergillosis?”

Why genomics — and why now?

Modern molecular tests such as PCR and DNA sequencing are becoming faster, cheaper and more accurate. Because of this, the NHS is increasingly exploring how genomic technologies can be used to improve diagnosis, monitoring and treatment across many diseases — including aspergillosis.

This year’s WAD meeting will start an open discussion between patients and professionals about which genomic and molecular tests are likely to matter most for people with aspergillosis in the years ahead.

Topics will include:

  • 🧠 Is there a “gene for aspergillosis”?
    Should people be tested for genetic susceptibility?

  • 💊 Genes and voriconazole dosing
    Can testing the CYP2C19 gene help personalise antifungal treatment?

  • 🦠 Tracking antifungal resistance
    How molecular testing of Aspergillus strains can help hospitals monitor resistance.

  • 🔬 Aspergillus PCR at NAC
    How PCR is already used to diagnose and monitor chronic aspergillosis.

🗣️ Patient voices at the heart of the meeting

As always, patient experience will be central to the day.

This year will include new patient stories, including Alison, who will talk about how her aspergillosis treatment led to the development of adrenal insufficiency, and what that has meant for her care and daily life.

“I don’t know anything about genetics — is this for me?”

Absolutely yes.

You don’t need any background in genetics to take part. Everything will be explained clearly, step by step, with minimal jargon.

Planned discussion topics include:

  • What do my Aspergillus PCR test results actually mean?

  • Is there really a “gene for CPA”?

  • Why do genes matter for antifungal dosing?

In fact, the more questions you ask — especially the “silly” ones — the better. The discussion from the day will be used to create a new patient leaflet, designed to help people better understand their diagnosis and test results.

✅ Registration is now open

🎟 Book your free place via Eventbrite:
👉 www.eventbrite.co.uk/e/world-aspergillosis-day-tickets-1980707139373

💻 Joining via Microsoft Teams

The meeting will be held online using Microsoft Teams, which you can download here:
👉 www.microsoft.com/en-gb/microsoft-teams/group-chat-software

If you haven’t used Teams before, we recommend doing a test call in advance. If you run into any problems setting things up, we’re very happy to help.

We hope you can join us for World Aspergillosis Day 2026 — to learn, to ask questions, and to help shape the future of aspergillosis care together.

by GAtherton

January–February 2026 Aspergillosis Papers (week 3)

Grouped by relevance and impact

🟥 HIGH IMPACT / PRACTICE-RELEVANT

(Most important for patients, clinicians, and services)

1. Chronic Pulmonary Aspergillosis (CPA): outcomes and mortality

Clinical Features and Mortality of Chronic Pulmonary Aspergillosis in Brazil
Open Forum Infectious Diseases, Jan 2026

Why this is important

  • Large multicentre cohort

  • Real-world data from TB-endemic, resource-limited settings

  • Directly relevant to global CPA burden, including post-TB disease

Key messages

  • CPA carries substantial long-term mortality

  • Tuberculosis is a major driver of CPA worldwide

  • Delayed diagnosis and limited antifungal access worsen outcomes

➡ This is one of the most important papers in the list for public health, service planning, and advocacy.

2. Invasive Aspergillosis in Intensive Care (including COVID-19)

Clinical spectrum of ICU-acquired invasive pulmonary aspergillosis according to SARS-CoV-2 infection
Eur J Clin Microbiol Infect Dis, Jan 2026

Why this is important

  • Large prospective multicentre ICU cohort

  • Builds on lessons from COVID-19 Associated Pulmonary Aspergillosis (CAPA)

Key messages

  • ICU-acquired aspergillosis remains common and deadly

  • COVID-19 patients are typically older and more severely ill

  • Early fungal testing in ICU is critical

➡ High relevance for intensivists, respiratory teams, and hospital policy.

3. Drug interactions in invasive aspergillosis

Concurrent administration of triazoles with chemotherapeutic and/or immunosuppressant agents
Mycopathologia, Jan 2026

Why this is important

  • Addresses real-world prescribing risk

  • Highly relevant to cancer, transplant, and haematology patients

Key messages

  • Triazole antifungals cause clinically dangerous drug–drug interactions

  • Requires specialist pharmacy oversight and monitoring

  • Not theoretical – directly affects patient safety

➡ High importance for clinicians and pharmacists, less so for patients directly, but critical for safe care.

🟧 MODERATE IMPACT / CLINICALLY INFORMATIVE

(Important, but narrower scope or smaller evidence base)

4. Aspergillosis beyond the “immunocompromised”

Pulmonary fungal infections in the immunocompetent host
Chest, Jan 2026 – Review

Why this matters

  • Challenges outdated assumptions

  • Useful for GPs and general physicians

Key messages

  • Serious fungal lung disease can occur without classic immune suppression

  • Chronic lung disease, viral infection, or exposure can be sufficient

  • Supports earlier fungal consideration when antibiotics fail

➡ Good educational review, especially for non-specialists.

5. Aspergillus species diversity and resistance

Beyond Fumigatus: a molecular portrait of clinical Aspergillus diversity
Antimicrobial Agents and Chemotherapy, Jan 2026

Why this matters

  • Advances understanding of non-fumigatus Aspergillus

  • Relevant to antifungal resistance

Key messages

  • Aspergillosis is caused by multiple species

  • Species identification may influence treatment success

  • Supports move toward precision mycology

➡ Important scientifically, indirect impact for patients (for now).

6. Minimally invasive treatment of aspergilloma

Minimally invasive management of a centrally located pulmonary aspergilloma
MMCTS, Jan 2026

Why this matters

  • Demonstrates evolving surgical approaches

  • Relevant to selected patients only

Key messages

  • Less invasive procedures may reduce surgical risk

  • Careful patient selection is crucial

➡ Clinically interesting, but case-based and niche.

🟨 LOW IMPACT / EARLY-STAGE / NICHE

(Useful context or future potential, limited immediate impact)

7. ABPA immunology and diagnostics (early-stage science)

Pathogen-specific IgE-reactive cytosolic allergenic epitopes of Aspergillus fumigatus
Ann Clin Microbiol Antimicrob, Jan 2026

Why this matters

  • Laboratory-based discovery research

Key messages

  • May improve future ABPA diagnostics

  • Potential foundation for targeted immunotherapy

➡ Promising but not practice-changing yet.

8. Voriconazole neurotoxicity (single case)

Voriconazole-associated peripheral polyneuropathy: A case report
Arch Argent Pediatr, Feb 2026

Why this matters

  • Highlights a rare but serious adverse effect

Key messages

  • Neurological symptoms on antifungals should not be ignored

  • Reinforces importance of monitoring during long-term therapy

➡ Low evidence level, but high awareness value.

9. Invasive aspergillosis in complex transplant oncology case

An Unforeseen Diagnosis After Liver Transplantation for Acute Liver Failure
Case Reports in Hepatology, Jan 2026

Why this matters

  • Illustrates diagnostic complexity in extreme immunosuppression

Key messages

  • Invasive aspergillosis can be rapidly fatal

  • Symptoms may be masked by other conditions

➡ Educational case, not generalisable.

10. Food enzyme safety (non-clinical)

Safety evaluation of the food enzyme aspergillopepsin I
EFSA Journal, Jan 2026

Why this matters

  • Addresses public concern rather than clinical disease

Key messages

  • Aspergillus-derived food enzymes are safe when regulated

  • Dietary exposure ≠ inhaled fungal spores

➡ Reassuring, but peripheral to aspergillosis care.

🔑 Overall “Most Important” Papers (Quick List)

Top tier

  1. CPA outcomes and mortality (Brazil cohort)

  2. ICU / COVID-19 associated invasive aspergillosis

  3. Triazole drug–drug interactions

Second tier
4. Fungal infection in immunocompetent hosts
5. Aspergillus species diversity & resistance

January–February 2026 Aspergillosis Papers – Source Links

🟥 High-impact / practice-relevant

  • Clinical Features and Mortality of Chronic Pulmonary Aspergillosis in Brazil: a Multicenter Cohort Study
    de Oliveira VF et al., Open Forum Infectious Diseases, Jan 2026
    🔗 https://pubmed.ncbi.nlm.nih.gov/41536616/

  • Clinical spectrum of ICU-acquired invasive pulmonary aspergillosis according to SARS-CoV-2 infection: a multicenter prospective cohort study
    Reizine F et al., European Journal of Clinical Microbiology & Infectious Diseases, Jan 2026
    🔗 https://pubmed.ncbi.nlm.nih.gov/41526761/

  • Concurrent Administration of Triazoles with Chemotherapeutic and/or Immunosuppressant Agents Known to Have Moderate-to-Severe Drug-Drug Interactions in Patients with Hematologic Malignancies Hospitalized for Invasive Aspergillosis
    Walsh TJ et al., Mycopathologia, Jan 2026
    🔗 https://pubmed.ncbi.nlm.nih.gov/41528615/

🟧 Moderate-impact / clinically informative

🟨 Lower-impact / niche / early-stage

  • Pathogen-specific IgE-reactive cytosolic allergenic epitopes of Aspergillus fumigatus for immunodiagnostic and immunotherapeutic applications against allergic aspergillosis
    Koundal P et al., Annals of Clinical Microbiology and Antimicrobials, Jan 2026
    🔗 https://pubmed.ncbi.nlm.nih.gov/41540426/

  • Voriconazole-associated peripheral polyneuropathy: A case report
    González BJ et al., Archivos Argentinos de Pediatría, Feb 2026
    🔗 https://pubmed.ncbi.nlm.nih.gov/40728252/

  • An Unforeseen Diagnosis After Liver Transplantation for Acute Liver Failure: Extranodal NK/T-Cell Lymphoma (includes invasive aspergillosis)
    Soares GL et al., Case Reports in Hepatology, Jan 2026
    🔗 https://pubmed.ncbi.nlm.nih.gov/41542139/

  • Safety evaluation of the food enzyme aspergillopepsin I from the genetically modified Trichoderma reesei strain DP-Nzq40
    EFSA Panel on Food Enzymes, EFSA Journal, Jan 2026
    🔗 https://pubmed.ncbi.nlm.nih.gov/41531469/

by GAtherton

What’s New in Aspergillosis Clinical Trials (Last ~4 Months)

An overview for patients and non-specialist readers — 19 January 2026

Over the past four months, research into aspergillosis — including chronic, allergic, and invasive forms — has continued across a range of clinical trials. These studies include treatments, diagnostics, and better ways to understand who gets sick and how best to manage it.

Below is a summary of the most relevant trials now active, recruiting, or updated recently. Whenever possible, we link to the official ClinicalTrials.gov record so you can see the details, eligibility criteria, locations, and contact information.

📋 Clinical Trials of Interest

1. Phase III Olorofim Trial for Invasive Aspergillosis

Study title: Olorofim Aspergillus Infection Study
Condition: Invasive aspergillosis (IA)
What it’s testing: A new antifungal drug called olorofim compared with liposomal amphotericin B followed by standard care.
Status: Active — not currently recruiting new patients but ongoing through 2026.
Official record: Olorofim Aspergillus Infection Study on ClinicalTrials.gov
Last updated: January 4, 2026
Why this matters: Olorofim is a completely new class of antifungal designed for patients whose infection is difficult to treat with standard drugs. It may offer an alternative for those with drug-resistant or treatment-intolerant infections.

2. Rezafungin in Chronic Pulmonary Aspergillosis (CPA)

Study title: Rezafungin for Treatment of Chronic Pulmonary Aspergillosis
Condition: Chronic pulmonary aspergillosis
What it’s testing: A long-acting echinocandin antifungal (rezafungin) that might reduce dosing frequency.
Status: Recruiting / active
Official record: Rezafungin CPA Trial on ClinicalTrials.gov
Why this matters: Current CPA treatments can require daily medication and prolonged therapy. Rezafungin’s once-weekly dosing could help reduce burden and hospital visits.

3. Combination Trial: Ibrexafungerp + Voriconazole (SCYNERGIA)

Study title: Evaluate Safety and Efficacy of Ibrexafungerp With Voriconazole in Invasive Pulmonary Aspergillosis
Condition: Invasive pulmonary aspergillosis
What it’s testing: Whether combining two antifungals works better than standard therapy alone.
Status: Active (ongoing)
Official record: SCYNERGIA Combination Trial on ClinicalTrials.gov
Why this matters: Some patients don’t respond well to single-agent treatment. Combination therapy may help in severe cases, especially where resistance is a concern.

4. PCR Diagnostic Study for Aspergillus fumigatus

Study title: PCR for Aspergillus Fumigatus in Blood and Bronchoalveolar Lavage Fluid
Condition: Aspergillosis (diagnostic focus)
What it’s testing: A blood and lung fluid PCR test to improve early detection of aspergillosis.
Status: Recruiting
Official record: PCR Aspergillus fumigatus Diagnostic Trial on ClinicalTrials.gov
First posted: 2 January 2026
Why this matters: Early diagnosis increases the chance of successful treatment. A reliable PCR test could allow clinicians to start antifungal therapy sooner.

🔎 What Else Is Ongoing?

There are other studies that include aspergillosis patients or Aspergillus exposure as part of broader research, such as:

  • All-of-Us Research Program fungal infection analysis — large observational work looking at fungal disease patterns in hundreds of thousands of people in the U.S., including aspergillosis. (Not a clinical trial per se but relevant to understanding how aspergillosis affects populations.)

  • Historic or related trials — e.g., older isavuconazole comparisons (e.g., NCT00412893) exist but are not newly updated.

🧠 What This Means for Patients

  • New antifungal drugs like olorofim and rezafungin are being tested in late-stage studies — these could expand treatment options in the future.

  • Combination therapies (e.g., ibrexafungerp + voriconazole) are being assessed to tackle difficult or resistant infections.

  • Improved diagnostics (e.g., PCR tests for Aspergillus fumigatus) are now being studied to help clinicians diagnose infections earlier and more accurately.

  • Not all trials are about treatment — some focus on better ways to detect infection or understand disease patterns, which are important for prevention and clinical practice.

🗓 How to Use These Links

Clicking a trial link takes you to the official ClinicalTrials.gov page, where you can often see:

  • Who can participate

  • Locations and contact information

  • Detailed eligibility criteria

  • Sponsor and trial timelines

If you have questions about joining a trial or how it applies to you specifically, always discuss this with your healthcare team.

by GAtherton