A Deadly Fungus That Kills Thousands a Year Hides in Hair Follicles

Scientists have just found how they could stop it. 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 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 nearly two dozen 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. Newsweek has contacted the study's authors for further comment.

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. 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. 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.