Researchers at the University of Exeter have identified a genetic mechanism in Candida auris, a lethal fungus resistant to most antifungal drugs, that could lead to new treatments. Using a novel infection model based on fish larvae, the team observed how the pathogen activates genes to scavenge iron during infection. This discovery offers hope for combating outbreaks that have forced hospital intensive care units to close.
Candida auris emerged as a global health threat in 2008, with its origins still unknown. The fungus has caused outbreaks in over 40 countries, including the UK, and is listed by the World Health Organization as a critical priority fungal pathogen. It poses a severe risk to critically ill patients, particularly those on ventilators, with a mortality rate of about 45 percent. Its resistance to all major antifungal drugs has made eradication challenging, leading to hospital closures and significant costs for health systems.
A study published in Communications Biology in 2025 marks a breakthrough in understanding the fungus. Led by NIHR Clinical Lecturer Hugh Gifford and Dr. Rhys Farrer from the University of Exeter's MRC Centre for Medical Mycology, the research used Arabian killifish larvae as a living host model. This approach overcame limitations of traditional models, as Candida auris thrives in high temperatures and salt, traits suggesting possible marine origins like tropical oceans.
During infection, the fungus forms elongated filaments to seek nutrients and activates genes for nutrient pumps that capture iron-scavenging molecules. Iron is vital for its survival, revealing a potential vulnerability. Gifford noted: "Since it emerged, Candida auris has wreaked havoc where it takes hold in hospital intensive care units. It can be deadly for vulnerable patients, and health trusts have spent millions on the difficult job of eradication. We think our research may have revealed an Achilles heel in this lethal pathogen during active infection."
Farrer added: "Until now, we've had no idea what genes are active during infection of a living host. We now need to find out if this also occurs during human infection. The fact that we found genes are activated to scavenge iron gives clues to where Candida auris may originate, such as an iron-poor environment in the sea. It also gives us a potential target for new and already existing drugs."
The findings, supported by Wellcome, the Medical Research Council, and NC3Rs, suggest repurposing drugs that target iron scavenging. Gifford emphasized: "We have drugs that target iron scavenging activities. We now need to explore whether they could be repurposed to stop Candida auris from killing humans and closing down hospital intensive care units." Dr. Katie Bates from NC3Rs praised the model: "This new publication demonstrates the utility of the replacement model to study Candida auris infection and enable unprecedented insights into cellular and molecular events in live infected hosts."
While further human studies are needed, this research provides a promising avenue against a pathogen that has defied conventional treatments.
