Most microbes that land on skin get wiped out within days. Candida auris, a drug-resistant fungus behind dangerous hospital outbreaks worldwide, does something far stranger: it recruits the body’s own immune system to help it stay put. New research from UC San Francisco, published in the journal Science, explains exactly how it pulls this off — and why hospitals have struggled for years to clear it from patients’ skin.
Key Takeaways
- C. auris binds to human hair roughly 30 times more readily than its close relative Candida albicans, and settles into hair follicles where it can persist for a month or longer.
- Rather than triggering the immune response that normally clears fungal skin infections, C. auris triggers a different signal that actually suppresses the skin’s defenses, effectively lowering its own guard.
- The fungus does this by exposing more of a cell-wall material called chitin when it senses skin-like conditions, which misdirects the immune response.
- This research was done primarily in mice, with supporting experiments in human skin cell cultures — direct evidence in human patients is still limited.
Why This Fungus Has Been So Hard to Get Rid Of
C. auris was first identified in Japan in 2009 and has since spread to hospitals and long-term care facilities around the world, killing an estimated 3,000 patients annually in the US alone through bloodstream infections, with reported mortality rates for those infections ranging from 30-70% depending on the patient population. What makes it a distinct problem is that it usually doesn’t make healthy people visibly sick — it can live quietly on a person’s skin for months, which is exactly what makes it so easy to unknowingly spread between patients in a hospital setting. Until now, no one fully understood why it clings on so persistently, and no method has reliably cleared it from skin in clinical practice.
How Researchers Cracked the Mechanism
The team compared C. auris directly against Candida albicans, a related fungus that also lives on human skin but gets cleared efficiently. Applied to mouse skin, C. albicans vanished within days. C. auris was still present a full 30 days later. Part of the explanation was mechanical: in lab tests, C. auris bound to human hair about 30 times more readily than C. albicans, and in mice it clustered specifically around hair follicles.
The bigger factor was what the immune system did in response. C. albicans triggered a signal called IL-17, which strengthens the skin’s protective barrier and helps kill the fungus — working the way a healthy immune response should. C. auris triggered a completely different signal, interferon-gamma, which is normally useful for fighting deeper infections but does close to the opposite of what’s needed on the skin’s surface — suppressing the very defense programs that would otherwise clear the fungus.
The Molecular Trick Behind It
Researchers traced the misdirection to the fungus’s outer cell wall. When grown under skin-like conditions — salty, nutrient-poor, at body temperature — C. auris exposed significantly more of a tough structural material called chitin (the same substance found in insect shells and crab exoskeletons) on its surface. That chitin exposure turned out to be the trigger for the unhelpful immune response: injecting purified chitin alone into mouse skin, with no fungus present, produced the same effect, and strains of C. auris engineered to display more or less chitin drew a correspondingly stronger or weaker immune reaction and colonized skin more or less as a result.
“Candida auris colonizes skin way better than most other fungi, setting it up to invade once the immune system is weakened,” said Dr. Eric Dean Merrill, the study’s first author, in a UCSF release. “The big clinical problem is that we have no effective way to remove it from the skin.” Co-senior author Dr. Suzanne Noble added that the team was surprised to find the fungus “actively uses its chitin to turn the skin into a perfect nest,” rather than the chitin exposure simply being incidental.
What This Doesn’t Confirm Yet
This mechanism was worked out primarily in mice, and while a supporting experiment using lab-grown human skin cells responded the same way, that’s suggestive rather than confirmatory — whether the same process drives persistence in actual human patients remains an open question the researchers themselves acknowledge. The study also focused on four major genetic lineages of C. auris, which may not capture the full diversity of strains currently circulating.
Why This Matters for Future Treatment
Dr. Ari Molofsky, another co-senior author, framed the bigger picture: “For most people, Candida auris hangs out on the skin and doesn’t cause any problems. It’s only when it reaches deeper tissues in medically vulnerable patients that it becomes dangerous. Understanding how it survives on the skin may help explain how it eventually causes serious infections.” The findings point toward two possible treatment directions worth pursuing in future research: drugs that could tilt the immune response away from the unhelpful interferon-gamma signal and toward the protective IL-17 response, or drugs that block the fungus’s ability to expose chitin in the first place. Neither approach has yet been shown to actually clear C. auris from human skin — but for the first time, researchers have a specific biological target to aim at.
Source: Merrill, E.D., Prudent, V., Basso, P., et al., including Molofsky, A.B. and Noble, S.M. (2026). The fungal pathogen Candida auris exposes chitin to trigger IFNγ and persist in hair follicles. Science, 393(6811), eadu6688. DOI: 10.1126/science.adu6688.