Scientists find a weak spot in deadly fungus that shut down hospital intensive care units

A deadly hospital fungus that resists nearly every antifungal drug may have an unexpected weakness. Researchers discovered that Candida auris activates specific genes during infection to hunt for nutrients it needs to survive. This insight came from a new living-host model that allowed scientists to watch the fungus in action. The findings could eventually lead to new treatments or allow current drugs to be repurposed.

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Scientists have identified a genetic mechanism that could point to new ways of treating a rare but deadly fungal infection that has forced multiple hospital intensive care units to shut down. The finding offers early hope against a pathogen that has been difficult to control and nearly impossible to treat once it spreads.

Candida auris is especially dangerous for people who are already critically ill, leaving hospitals highly exposed to outbreaks. Although the fungus can exist on the skin without causing symptoms, patients who depend on ventilators face a much greater risk. Once infection occurs, about 45 percent of patients die, and the fungus is resistant to all major types of antifungal drugs. This resistance makes treatment extremely challenging and allows the pathogen to persist in hospital wards.

The infection was first detected in 2008, and its origin is still unknown. Since then, outbreaks have been reported in more than 40 countries, including the UK. Candida auris, also called Candidozyma auris, is now recognized as a serious global health threat and appears on the World Health Organization's critical priority fungal pathogens list. In the UK, reported cases have continued to rise steadily.

Researchers at the University of Exeter have now taken a major step forward by examining how genes are activated during Candida auris infection. This marks the first time such genetic activity has been studied in a living host using an approach based on fish larvae. The study was published in the Nature portfolio journal Communications Biology and was supported by Wellcome, the Medical Research Council (MRC), and the National Center for Replacement, Reduction and Refinement (NC3Rs).

The researchers say the results could help identify a biological target for new antifungal treatments or even allow existing drugs to be reused, if the same genetic behavior is confirmed during infection in humans.