Deadly Fungus Kills Thousands Every Year. Scientists Found Where It Hides

A drug-resistant fungus called Candida auris, which has claimed the lives of thousands of hospital patients annually in the United States, has been discovered to survive on human skin by manipulating the body's immune system. Dean Merrill, a dermatologist and professor at the University of California, San Francisco (UCSF) and the lead researcher in the recent study, explained that Candida auris is exceptionally adept at colonizing skin compared to most other fungi, effectively setting the stage for subsequent invasion once the immune system has been weakened.

Regrettably, there is currently no effective means to eradicate Candida auris from the skin. This particular fungus is currently spreading across the United States, with its presence confirmed in more than half of the states, as reported by the Centers for Disease Control and Prevention (CDC).

Candida auris, a type of yeast, was initially identified in Japan in 2009 and has since proliferated in hospitals and long-term care facilities worldwide. Typically harmless on the skin, it can prove fatal if it enters the bloodstream, particularly for susceptible individuals. The CDC estimates that the fungus kills approximately 3,000 patients each year in the U.S. alone, and it poses a significant challenge to treat due to the resistance exhibited by certain strains against common antifungal drugs.

The reasons behind Candida auris's persistence on human skin, which distinguishes it from other fungi that are rapidly cleared by the immune system, were previously unknown. To unravel this mystery, a team at UCSF conducted a study published in Science, comparing Candida auris with Candida albicans, a common fungus that is typically cleared by healthy immune systems within days.

The researchers discovered that Candida auris thrives in hair follicles, unlike Candida albicans, which rapidly disappears from the skin. The two fungi elicit distinct immune responses. Candida albicans triggers the secretion of a signal named IL-17, prompting the skin to renew its surface and enhance its natural antifungal defenses, effectively clearing the infection independently.

Conversely, Candida auris triggers interferon gamma, a signal more commonly associated with virus combat rather than fungi, which is ineffective in this context. Candida auris achieves this by altering its cell wall to expose more chitin—a molecule that prompts nearby immune cells to release interferon gamma around hair follicles.

In response to the interferon gamma, the skin's antifungal defenses, including the beneficial IL-17 response, are suppressed, and the normal turnover of hair follicle cells slows down. This creates a protected environment where Candida auris can thrive undetected and undisturbed.

According to Suzanne Noble, a professor of microbiology at UCSF and co-senior author of the paper, "Chitin is prevalent in nature, so it's not as if human skin never encounters it. However, we were astonished to discover that Candida auris actively utilizes its chitin to transform the skin into an ideal nest." The findings suggest potential strategies to eliminate Candida auris from the skin.

One approach could involve drugs that alter the immune response from interferon gamma to IL-17, reinstating the skin's natural antifungal clearing process, even in the presence of this formidable fungus. Another strategy could involve blocking chitin itself, thereby preventing the fungus from triggering the interferon gamma response in the first place.

Overall, the study provides a novel framework for comprehending how microbes can coexist with the human body and subsequently turn dangerous.