Candida auris exposes chitin to stay in the hair follicle

Candida auris is on the World Health Organization priority list not because it is unusually virulent, but because it is hard to get rid of. It persists on patients' skin and on ward surfaces, tolerates some antifungal drugs and causes outbreaks that ordinary cleaning does not stop. Why skin in particular went unanswered for a long time.

A team at the University of California, San Francisco, led by Eric Dean Merrill, compared skin colonisation in mice by Candida auris and by the better-studied Candida albicans. The difference turned out to be qualitative rather than quantitative. Candida auris persisted longer, gathered around hair follicles and bound directly to hair.

The immune reaction is the interesting part. Candida albicans triggered a type 3 response involving interleukin 17 — the one that clears the fungus. Candida auris triggered a different type, driven by interferon gamma and directed at the hair follicles. The effect was the opposite of what one would expect: interferon gamma acted on keratinocytes and repressed their antifungal defence programmes, which made colonisation easier.

The authors also showed what the fungus uses to provoke that response. On contact with cues associated with skin, Candida auris increases the exposure of chitin in its cell wall. Chitin is the signal here — it is what triggers type 1 immunity, and that in turn favours fungal persistence. The result therefore adds up to a mechanism in which the pathogen itself selects which response it will draw.

The limits of the result are worth stating. The work was done in mice, and mouse skin and mouse hair follicles differ from human ones. Showing that interferon gamma favours colonisation is not yet a therapeutic indication — blocking that pathway in a patient with a severe infection would have consequences reaching far beyond the skin.

The practical significance is concrete nonetheless. A patient's skin has until now been treated mainly as a surface to be disinfected. This work shows it is better understood as a habitat with its own structure, and that the hair follicle is a niche within that habitat which a disinfectant may simply not reach. It changes the question asked during a hospital outbreak: not what to wash with, but where the fungus sits.

For a reader outside medicine there is a broader conclusion. Chitin — the same polymer that builds the cell wall of edible fungi and makes them harder to digest — is at the same time one of the most important signals by which the body recognises a fungus. What the immune system sees depends on how much of that chitin the fungus puts on show.

Evidence status — 29 August 2026

Published in Science on 6 August 2026, the study compared skin colonisation by Candida auris and C. albicans in mice. C. auris persisted around hair follicles, exposed more chitin and triggered a type 1, interferon-gamma-driven response; signalling in keratinocytes suppressed part of the epithelial antifungal programme and favoured colonisation. This is a coherent mechanism in a mouse model, not confirmation of an identical process on human skin or a reason to block interferon clinically. It matters for infection control because it frames the follicle as a protected biological niche, not merely part of a surface to disinfect.