This Hospital Fungus Has a Surprising Hiding Place

C. auris appears remarkably well adapted to living on the skin. We found that it binds directly to hair and preferentially settles into hair follicles, where it can persist for weeks, whereas the related fungus C. albicans is rapidly cleared.

But C. auris does more than find a favorable place to hide. When it encounters conditions that mimic the skin, such as body temperature, salt, and limited nutrients, it dramatically remodels its cell wall and exposes chitin, a structural material that is normally relatively hidden from the immune system—chitin changes the “flavor” of the immune response.

C. albicans triggers an IL-17–dominated response that activates skin cells to proliferate, strengthen the barrier, produce antimicrobial molecules, and ultimately eliminate the fungus.

C. auris, in contrast, drives an Interferon-gamma (IFNγ)–dominated immune response that suppresses some of those protective programs in skin cells and paradoxically creates an environment in which the fungus can persist.

So rather than simply escaping detection, C. auris appears to exploit the immune response to help establish a long-term home in the hair follicle. That may help explain one of the most challenging features of this pathogen: people can remain silently colonized on their skin for months, creating opportunities for transmission and, in vulnerable patients, invasive infection.

Hair follicles provide C. auris with both a physical and an immune niche for long-term colonization. There is ample surface area between the hair shaft and surrounding skin cells for the fungus to attach, and we found that C. auris binds particularly well to hair.

Hair follicles are also immune hubs that are naturally enriched for type 1 immune cells—the same type of immune response that our work found paradoxically favors C. auris persistence. Together, these features may make the hair follicle an especially favorable home for long-term colonization.

Once C. auris moves beyond the skin surface and enters deeper tissues or the bloodstream, the role of the immune response changes dramatically. On the skin, we found that IFNγ–driven type 1 immunity paradoxically helps the fungus persist; during invasive infection, however, the same cytokine becomes protective, likely in part by activating macrophages that help control the fungus. This highlights how the location of an infection can fundamentally change whether an immune response helps the host or the pathogen.

C. auris can silently colonize the skin for months, so detecting carriers requires intensive screening. Our study shows that the fungus is remarkably well adapted for this lifestyle: it binds to hair, establishes itself within hair follicles, and remodels its cell wall in response to skin conditions to redirect the immune response in ways that favor persistence. This combination sets the stage for asymptomatic spread and outbreaks in healthcare facilities. In long-term care settings, where patients often have serious medical conditions and other risk factors, a fungus that is harmlessly colonizing the skin can then become a dangerous invasive pathogen.

Our findings identify several potential targets, although these approaches still need to be tested. One is the fungal cell wall: reducing chitin production or preventing C. auris from exposing chitin could make it harder for the fungus to establish persistent colonization. Another is the local immune response—selectively reducing the type 1/IFNγ pathway that favors persistence in the skin, or enhancing protective IL-17–mediated immunity, could potentially shift the balance toward fungal clearance.