BIONEWS
Candida auris, a drug resistant fungus that kills roughly 3,000 U.S. patients a year, hides in hair follicles and flips local immunity off, a new Science paper reports.
Every tool hospitals use to scrub Candida auris off a patient's skin runs into the same wall. Chlorhexidine baths, antifungal washes, and repeat cultures all face one limit: the fungus lives where soap cannot reach, inside the hair follicle, and tells the surrounding tissue to leave it alone.
A new [study reported in Science this week](https://www.genengnews.com/topics/infectious-diseases/candida-auris-persists-in-hair-follicles-hijacks-immune-signaling/) gives the first concrete biological handle on a problem clinicians have run out of answers for. C. auris kills roughly 3,000 U.S. patients a year in hospitals and long-term care facilities, the report says, citing public health estimates. The existing decolonization playbook does not reliably clear the skin.
The paper reframes the pathogen's persistence. The clinical conversation has long centered on drug resistance. The new finding points somewhere else: a specific anatomical niche and a specific immune-redirect that lets the fungus stay there.
In mouse skin, C. auris settles inside hair follicles, in higher numbers and for longer stretches than the far more common skin fungus Candida albicans, which is cleared within days. The team used volumetric quantitative confocal microscopy to watch the fungus stake out that niche rather than sit on the surface. The follicle is the visual anchor: a place the antiseptic cannot reach.
"The big clinical problem is that we have no effective way to remove it from the skin," said Dean Merrill, a dermatologist and professor at UC San Francisco. The mouse work now offers a reason current scrubs fall short: the target is buried in a structure surface antiseptics barely reach.
The chain runs through the fungus's outer wall. C. auris remodels its cell wall to expose more chitin, the same structural polymer that gives fungal cell walls their rigidity. That chitin exposure is the trigger.
In normal skin, a closely related fungus like C. albicans triggers a type 3/17 immune response, the skin-clearing program driven by IL-17A. C. auris triggers something different. It expands a set of immune cells (cDC1 dendritic cells, Tc1 and Th1 T cells) and pushes the local response toward interferon-gamma, or IFNγ, around the hair follicle.
IFNγ then acts directly on the follicle's keratinocytes, the structural cells that build the skin barrier. It suppresses the IL-17A-driven program those cells would normally use to maintain the barrier and push out fungi. The result is a niche that the skin's normal clearing machinery has been switched off inside.
In mice with defects in the relevant cytokine signaling, IFNγ promoted C. auris persistence in the skin even though it still played a protective role during deeper infection. The same molecule that helps the body fight off a bloodstream infection appears to help the fungus keep its grip on a hair follicle.
The findings are mouse data, not human. The IFNγ link is a correlation inside this system, not yet a proven causal drug target in patients. Hospital decolonization protocols have not changed because of this paper, and clinicians are not yet testing IFNγ blockers as a skin-clearance strategy.
The work also did not address how the chitin-exposed wall flips the local response, only that it does. That is the next experimental question, and the most likely handle for a future therapy. Drugs that block IFNγ signaling, or that mask the chitin signal before it reaches the follicle, are the obvious targets, though none has been validated for C. auris skin infection.
A blood test for IFNγ activity in patients with persistent C. auris skin colonization would tell researchers whether the mouse pathway is even operative in people. The cleanest next step is a deliberate test of an existing IFNγ blocker in colonized patients, off-label, as a probe.
The clinical dead-end Merrill named has not moved. The next move in the field is to find out whether blocking the redirected signal, rather than scrubbing the surface, is what finally clears the skin.