IPM Take
A disease does not need thousands of cases to expose a surveillance failure.
Cladophialophora bantiana is extraordinarily rare, but when it reaches the brain the consequences can be devastating. A reference laboratory is now seeing substantially more detections, yet the United States lacks the national reporting infrastructure needed to determine whether incidence is genuinely changing, where exposure occurs or who is at greatest risk.
Executive Summary
CDC researchers report a substantial increase in molecular detection of Cladophialophora bantiana, a neurotropic fungus that predominantly causes brain abscesses.
A University of Washington reference laboratory identified 48 confirmed and one probable infection between 2009 and July 2026, originating from 21 states and the District of Columbia. Eight cases were detected in 2024 and 14 in 2025.
After accounting for growth in the number of central nervous system samples submitted to the laboratory, the detection rate rose by approximately 210% by 2025 compared with the 2017–2023 average, and CDC describes the overall frequency as having increased roughly fourfold between 2023 and 2025.
The reason is unknown. There is no routine national surveillance for the fungus, its environmental reservoir is poorly understood and around half of previously reported patients have not had a known immunocompromising condition.
Why it matters
- Clinicians: The fungus should enter the diagnostic differential for unexplained brain abscesses, including in patients without obvious immune suppression.
- Laboratories: Broad-range fungal PCR and sequencing may be crucial when conventional microbiology does not identify a cause.
- Public authorities: Systematic reporting is needed before an apparent increase can be understood epidemiologically.
Public-health surveillance is built to see common events efficiently. Rare infections test whether it can notice the unusual before the unusual becomes a pattern.
Cladophialophora bantiana sits at the extreme end of that problem. The fungus is uncommon enough that most clinicians will never diagnose a case, yet serious enough that infection has historically carried a reported case-fatality rate of 60–70%. It has a particular affinity for the central nervous system, where it can produce brain abscesses in immunocompromised patients but also in people with no obvious immune defect.
Now a laboratory signal has changed.
The University of Washington’s molecular reference laboratory identified only one to five cases annually for many years. Eight were detected in 2024 and 14 in 2025. Even after researchers adjusted for increasing numbers of CNS samples sent for fungal PCR, the rate had risen substantially. CDC characterises the frequency of detection as increasing roughly fourfold between 2023 and 2025.
Those figures deserve attention without sensationalism. This is not evidence of a contagious national outbreak, and C. bantiana is not known to spread routinely between people. The absolute number remains very small, and the dataset comes from one reference laboratory rather than a comprehensive national surveillance system.
That last point is precisely the problem.
Because routine national reporting does not exist, investigators cannot easily determine whether the rise reflects changing environmental exposure, broader geographic recognition, diagnostic behaviour, climate-related factors, evolving fungal biology or something else entirely. The environmental reservoir itself remains poorly characterised, while inhalation and direct inoculation after skin injury are suspected routes of acquisition.
The diagnostic challenge compounds the uncertainty. Brain abscesses can have multiple bacterial, fungal and parasitic causes, and rare moulds are not always identified through routine methods. Broad-range fungal PCR, which amplifies fungal genetic material without requiring clinicians to identify the organism in advance, can reveal pathogens conventional testing misses.
For patients, speed matters. Treatment usually involves combination antifungal therapy, often alongside surgical drainage or excision when feasible. Yet evidence is limited because the infection is so rare. There is no large clinical-trial literature capable of telling clinicians exactly which regimen is best.
This is where surveillance and research become inseparable. More systematic reporting would allow investigators to understand exposure history, geography, patient characteristics, outcomes and treatment. Without that, every institution sees a peculiar case while nobody sees the pattern.
Rare diseases are easy for public-health systems to ignore because the denominator never becomes politically impressive.
A fungus that kills a large proportion of the people it infects does not need to become common before the unanswered questions matter.
