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A drug-resistant fungus that kills thousands of hospital patients in the U.S. every year survives on human skin by hijacking the body's immune response, scientists have just discovered.
"Candida auris colonizes skin way better than most other fungi, setting it up to invade once the immune system is weakened," Dean Merrill, a dermatologist and assistant professor at the University of California, San Francisco (UCSF) and study lead, said in a statement. "The big clinical problem is that we have no effective way to remove it from the skin."
The fungus is currently sweeping through the U.S., having been detected in over half of the states this year, according to the Centers for Disease Control and Prevention (CDC). Their figures show that Candida auris screenings had been reported across multiple states as of the week ending July 25, 2026.
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A Silent but Deadly Threat
Candida auris, a kind of yeast, was first identified in Japan in 2009 and has since spread to hospitals and long-term care facilities worldwide. It typically lives harmlessly on the skin, but if it enters the bloodstream, it can turn deadly, especially for the most vulnerable. The fungus kills an estimated 3,000 patients a year in the U.S. alone, and it is notoriously difficult to treat because many strains resist common antifungal drugs.
Until now, scientists did not fully understand why C. auris clings to the skin so persistently while other fungi are cleared quickly by the immune system. The new study, published in Science and led by the team at UCSF, set out to answer that question.
To find out what sets C. auris apart, the researchers compared it with Candida albicans, a common fungus that healthy immune systems typically clear within days. In experiments with mice, C. albicans disappeared quickly. C. auris, however, persisted—taking refuge deep inside hair follicles.
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The two fungi triggered very different immune responses. C. albicans set off a signal called IL-17, which prompted the skin to renew its surface and ramp up its natural antifungal defenses, practically clearing the infection on its own. C. auris, by contrast, triggered interferon gamma, a signal more typically associated with fighting viruses rather than fungi, which is of little use here.
"Candida auris is an emerging, drug-resistant fungus that can live silently on the skin for months, particularly in patients in hospitals and long-term care facilities," Merrill told Newsweek. "This persistent colonization is important because it allows the fungus to spread from person to person and, in medically vulnerable patients, can precede life-threatening invasive infection. Our study set out to understand why C. auris is so good at persisting on the skin.
"We found that it is remarkably adapted to this environment: it binds directly to hair, preferentially colonizes hair follicles, and responds to skin-associated cues by remodeling its cell wall and exposing chitin."
Rewiring the Skin’s Defenses
C. auris achieves this by altering its own cell wall to expose more of a molecule called chitin.
That exposed chitin prompted nearby immune cells to release interferon gamma around the hair follicle. In turn, the interferon gamma suppressed the skin's antifungal defenses, including the prized and protective IL-17 response, and slowed the normal turnover of hair follicle cells.
The result was a buildup of older, damaged cells—creating a sheltered niche where the fungus could thrive largely undetected and undisturbed.
"Chitin is widespread in nature, so it's not like 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 professor of microbiology at UCSF and co-senior author of the paper, in a statement.
The findings point to possible strategies for clearing the fungus from the skin.
One option could involve drugs that shift the immune response away from interferon gamma and toward IL-17, restoring the skin's natural antifungal clearing process, even in the face of such a tricky fungus to combat. Another could involve blocking chitin itself, preventing the fungus from triggering the interferon gamma response in the first place.
More broadly, the researchers say their work offers a new framework for understanding how microbes can quietly coexist with the human body before turning dangerous.
"Our hope is that understanding how C. auris establishes and maintains this persistent skin reservoir will give us new ways to eliminate it," Merrill added. "There are currently no reliable approaches to clear C. auris from colonized skin, but our findings identify several potential points of intervention—including the fungal cell wall itself and the balance between IFNγ-driven type 1 immunity and IL-17-mediated protective barrier immunity.
"Ultimately, developing therapies that disrupt this fungus–immune interaction and restore effective antifungal defenses could help clear colonization, reduce transmission in healthcare settings, and potentially prevent invasive infections in the most vulnerable patients."
Reference
Merrill, E. D., Noble, S. M., et al. (2026). The fungal pathogen Candida auris exposes chitin to trigger IFNγ and persist in hair follicles. Science. https://dx.doi.org/10.1126/science.adu6688.
Contact Newsweek editors on this story: Kara Dolman and Gray R. Thomas
Update, 8/11/2026 11:57 a.m. ET: This article was updated with comment from Dean Merrill.
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