A lethal, drug-resistant hospital fungus might lastly have a weak point—and scientists assume they’ve discovered it.
Researchers have recognized a genetic course of that would open the door to new therapies for a harmful fungal an infection that has repeatedly pressured hospital intensive care items to shut. The invention gives recent hope in opposition to a pathogen that has been troublesome to regulate and even tougher to deal with.
Candida auris poses a critical menace to people who find themselves already critically unwell, making hospitals significantly weak to outbreaks. Though the fungus can exist harmlessly on the pores and skin of many individuals, sufferers who depend on ventilators face a a lot greater threat of an infection. As soon as it takes maintain, the illness kills round 45 per cent of these contaminated and might face up to each main class of antifungal treatment. This mixture has made it extraordinarily difficult to remove from hospital wards as soon as it spreads.
A worldwide well being menace on the rise
Candida auris was first recognized in 2008, and scientists nonetheless have no idea the place it initially got here from. Since its discovery, outbreaks have been reported in additional than 40 international locations, together with the UK. The fungus, also referred to as Candidozyma auris, is now acknowledged as a worldwide well being menace and seems on the World Well being Group’s crucial precedence fungal pathogens checklist. Within the UK, case numbers have continued to climb over time.
Learning an infection in a dwelling host
For the primary time, a crew on the College of Exeter has intently examined how Candida auris prompts its genes throughout an infection utilizing an revolutionary experimental mannequin primarily based on fish larvae. The analysis was printed within the Nature portfolio journal Communications Biology and acquired help from Wellcome, the Medical Analysis Council (MRC), and the Nationwide Middle for Alternative, Discount and Refinement (NC3Rs).
The outcomes recommend a promising path towards figuring out a organic goal that may very well be used to develop new antifungal medication or adapt current ones, offered the identical genetic exercise happens throughout an infection in people.
The work was co-led by NIHR Scientific Lecturer Hugh Gifford from the College of Exeter’s MRC Middle for Medical Mycology (CMM). He stated: “Because it emerged, Candida auris has wreaked havoc the place it takes maintain in hospital intensive care items. It may be lethal for weak sufferers, and well being trusts have spent tens of millions on the troublesome job of eradication. We expect our analysis might have revealed an Achilles heel on this deadly pathogen throughout energetic an infection, and we urgently want extra analysis to discover whether or not we are able to discover medication that focus on and exploit this weak point.”
Why a brand new mannequin was wanted
One long-standing problem in finding out Candida auris is its means to outlive excessive temperatures. Mixed with its unusually robust tolerance to salt, this has led some scientists to take a position that it could have originated in tropical oceans or marine animals. These traits have additionally made it tougher to review utilizing conventional laboratory fashions.
To beat this, the Exeter researchers developed a brand new system utilizing Arabian killifish, whose eggs are capable of survive at human physique temperature. This allowed the crew to watch the an infection course of in a dwelling host below practical situations.
Genetic clues to survival and unfold
In the course of the research, the researchers noticed that Candida auris can shift into elongated fungal buildings referred to as filaments, which can assist it seek for vitamins contained in the host.
In addition they tracked which genes have been turned on and off throughout an infection, highlighting potential weaknesses. A number of of the activated genes are concerned in producing nutrient pumps that seize iron-scavenging molecules and pull iron into fungal cells. Iron is important for survival, and this dependence might signify a crucial vulnerability.
Co-senior writer Dr. Rhys Farrer from the College of Exeter’s MRC Centre for Medical Mycology stated: “Till now, we’ve had no concept what genes are energetic throughout an infection of a dwelling host. We now want to seek out out if this additionally happens throughout human an infection. The truth that we discovered genes are activated to scavenge iron offers clues to the place Candida auris might originate, resembling an iron-poor surroundings within the sea. It additionally offers us a possible goal for brand spanking new and already current medication.”
Hope for future therapies
Dr. Gifford, who additionally works as a resident doctor in intensive care and respiratory medication on the Royal Devon & Exeter Hospital, emphasised the potential medical affect of the findings. He stated: “Whereas there are a selection of analysis steps to undergo but, our discovering may very well be an thrilling prospect for future therapy. We’ve medication that focus on iron scavenging actions. We now have to discover whether or not they may very well be repurposed to cease Candida auris from killing people and shutting down hospital intensive care items.”
The Arabian killifish larvae mannequin was developed with help from an NC3Rs venture grant as an alternative choice to utilizing mouse and zebrafish fashions, that are generally employed to review how pathogens work together with their hosts.
Dr. Katie Bates, NC3Rs Head of Analysis Funding, stated: “This new publication demonstrates the utility of the alternative mannequin to review Candida auris an infection and allow unprecedented insights into mobile and molecular occasions in reside contaminated hosts. This can be a good instance of how revolutionary various approaches can overcome key limitations of conventional animal research.”
Reference: “Xenosiderophore transporter gene expression and clade-specific filamentation in Candida auris killifish (Aphanius dispar) an infection” 19 December 2025, Communications Biology.
DOI: 10.1038/s42003-025-09321-z
