Infection control teams have spent a decade asking the same question about Candida auris: why can it not be scrubbed off? Patients colonized with the drug-resistant fungus carry it on their skin without symptoms, sometimes for months, and no approved treatment reliably clears it. When they transfer between facilities, the fungus travels with them.
Researchers at UC San Francisco now report an answer that is more unsettling than simple stubbornness. In mice, C. auris takes refuge inside hair follicles and reshapes the skin's immune response so those defenses work in its favor.
The study, published in Science on August 6, compared C. auris directly against Candida albicans, a common relative that healthy skin clears within days.
Days Versus Weeks
The comparison was deliberately plain. Both yeasts were applied to the shaved but undamaged back skin of mice. C. albicans vanished within days. C. auris was still there weeks later, and repeat applications did not change the pattern.
Tissue analysis showed where it had gone. Clusters of C. auris sat inside hair follicles, clinging to the shaft, the opening, and the follicle cavity, while C. albicans largely stayed on the flat skin surface. Removing hair with depilatory cream sharply reduced the fungal burden, and a dish experiment made the attraction explicit: human hair fragments incubated with each yeast picked up far more C. auris.
The team reached these conclusions using mouse genetics, fungal genetics, single-cell RNA sequencing, and volumetric confocal microscopy, and the full paper is indexed in PubMed.
"Candida auris colonizes skin way better than most other fungi, setting it up to invade once the immune system is weakened," said Dean Merrill, a UCSF dermatologist and first author, in the university's announcement. He added that the central clinical problem is the absence of any effective way to remove it from the skin.
The Immune Signal That Works Backward
The mechanism is where the study gets strange. The two fungi provoked opposite immune responses.
C. albicans triggered interleukin-17, a signal that renews the skin surface and ramps up antifungal defenses, clearing the infection. C. auris instead triggered interferon gamma, a messenger more commonly associated with fighting viruses.
It did this by remodeling its outer cell wall to expose more chitin, the structural material found in fungal walls and insect shells. That exposure prompted nearby immune cells to release interferon gamma around the follicle. The interferon gamma then suppressed IL-17 and slowed the natural replacement of hair follicle cells, allowing older, damaged cells to accumulate and creating a sheltered pocket where the fungus could sit largely undisturbed.
Turning that immune signal up or down in mice raised or lowered the fungal burden, tying the reaction directly to the fungus staying put.
"Chitin is widespread in nature, so it's not like the human skin never encounters it, but we were surprised to see that C. auris actively uses its chitin to turn the skin into a perfect nest," said Suzanne Noble, a UCSF professor of microbiology and co-senior author.
What This Does Not Establish
The mechanistic work was done in mice, and the distinction matters more than usual here. Mouse skin is far denser in hair follicles than most human skin, and the armpits and groin, where C. auris is typically found on patients, were not the anatomic focus of these experiments.
The finding does not mean that every person carrying C. auris has fungus living inside individual hair follicles. It identifies a niche and a mechanism in an animal model that plausibly explains a clinical observation, which is a different claim.
It is also worth being precise about who is at risk. Nearly all confirmed infections occur in people who are already seriously ill: patients on ventilators, those with central lines, feeding tubes or urinary catheters, and residents of long-term care facilities. Healthy people, including healthcare workers, are rarely colonized, and the CDC says screening family members is usually unnecessary. This is a story about facility infection control, not household hygiene.
Earlier work established the clinical stakes of skin carriage. Roughly 95 percent of colonized patients carry the fungus on the skin, and in one intensive care study, about a quarter developed bloodstream infection within 60 days. National figures are lower and cover a broader population: CDC surveillance of more than 21,000 colonized US patients from 2016 to 2023 found that 6.9 percent later had a positive clinical specimen, with 2.8 percent from blood. Either way, colonization precedes invasive disease.
Where a Treatment Might Come From
The practical payoff, if it arrives, would be decolonization, meaning a way to actually remove the fungus from a patient's skin rather than isolating them indefinitely.
Merrill has pointed to two directions. One would use drugs that tilt the immune response away from interferon gamma and back toward IL-17, restoring the skin's normal clearing process. Another would block chitin so the fungus cannot amplify the interferon gamma signal in the first place.
Both remain hypotheses. No such drug exists, and the immune signals involved are not narrow targets. Interferon gamma and IL-17 are central to defense against many pathogens, and deliberately rebalancing them in a critically ill patient is not a minor intervention.
The researchers also frame the work more broadly as a case study of how a microbe can coexist quietly with a host for long stretches before becoming pathogenic. That framing is likely to outlast any specific drug target the study produces.
Families with a relative in intensive care or a nursing home should ask about the facility's infection control practices, screening protocols, and cleaning procedures for shared equipment rather than about anything they can do at home.
Key Questions Answered
What did the researchers discover?
In mice, Candida auris persisted on the skin by settling into hair follicles and exposing chitin, which triggered interferon gamma and suppressed the skin's normal antifungal response.
Was this studied in people?
No. The mechanistic experiments used mouse models, fungal and mouse genetics, single-cell sequencing, and microscopy. Human colonization was not directly examined.
Does everyone with C. auris have it inside their hair follicles?
That has not been shown. The follicle niche was identified in mice, and mouse skin differs substantially from human skin in follicle density.
Who is actually at risk?
Almost exclusively, patients who are already seriously ill, particularly those with ventilators, central lines or catheters, and residents of long-term care facilities.
Can it be treated?
Infections can often be treated, though nearly all isolates are resistant to fluconazole. Skin colonization is the part that cannot currently be cleared.
What should families ask about?
Infection control practices at the facility, including screening protocols, isolation procedures, and the cleaning of shared equipment.
