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.