This creepy discovery could leave you scratching your head.
A new study found that a deadly fungus can burrow deep into hair follicles, rewire the immune system and transform human skin into what one researcher described as a “perfect nest” for infection.
And the threat may be closer than you think. Cases of the superbug have been reported in more than two dozen states this year alone — including areas just across the river from New York City.
Discovered in Japan in 2009 and first identified in the US in 2016, Candida auris is a type of yeast that can enter the bloodstream and travel throughout the body.
The fungus is primarily transmitted in healthcare settings like hospitals and nursing homes, where it can linger on contaminated surfaces for weeks at a time.
Some strains of the fungus are resistant to all major classes of antifungal medications, which is why the Centers for Disease Control and Prevention has labeled C. auris an “urgent antimicrobial resistance threat.”
For most people with healthy immune systems, the pathogen doesn’t cause serious illness. But they can still harbor the fungus and unknowingly pass it along to people at greater risk.
In fact, C. auris can survive silently on the skin for months without causing symptoms. That makes it different from other fungi, such as Candida albicans, which the immune system usually clears quickly.
In the latest study, researchers at the University of California, San Francisco sought out to understand why. In lab experiments, they infected mice with both fungi. They found that C. albicans disappeared within days, while C. auris remained, taking refuge inside hair follicles.
The researchers also discovered that the two fungi triggered dramatically different immune responses.
When the immune system encountered C. albicans, it activated a response called IL-17, which helps repair the skin’s surface and strengthens the body’s natural defenses against fungi, allowing the infection to be cleared.
But C. auris spurred a different reaction. Instead of triggering the same antifungal response, it activated interferon gamma, an immune signal usually used to fight viruses.
The fungus appeared to pull this off by altering the structure of its outer wall, exposing more of a molecule called chitin. This prompted nearby immune cells around the hair follicle to activate and release interferon gamma.
That response worked against the skin’s normal fungal defenses. It also slowed the replacement of old hair follicle cells, allowing damaged cells to accumulate and creating an environment where C. auris can survive and multiply.
“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,” Dr. Suzanne Noble, a professor of microbiology at UCSF and co-senior author of the study, said in a press release.
The big challenge for scientists is that there is currently no reliable way to completely remove C. auris from the skin. But the new findings could point to potential ways to control the fungus.
For now, C. auris remains difficult to treat, with doctors sometimes needing to combine multiple antifungal medications to clear infections.
Fortunately, for most people, the fungus remains on the skin and does not cause serious illness. Many carriers experience no symptoms at all, but when an infection does occur, signs can include fever, chills, fatigue, low blood pressure and a rapid heart rate, according to the Cleveland Clinic.
“It’s only when it reaches deeper tissues in medically vulnerable patients that it becomes dangerous,” said Dr. Ari Molofsky, an immunologist, UCSF professor and co-senior author of the study. “Understanding how it survives on the skin may help explain how it eventually causes serious infections.”
Experts say the true fatality rate of C. auris is difficult to gauge because many infected patients already have underlying conditions that increase their risk of severe illness.
The CDC estimates that up to 60% of people with C. auris infections have died, with the fungus contributing to roughly 3,000 deaths in the US each year.
So far in 2026, about 3,000 cases of the superbug have been documented across 23 states, including New Jersey. Texas has recorded the most cases, with more than 700 as of mid-July.
