Hospital rooms are meant to be places of recovery. But in intensive care units, a stubborn fungus called Candida auris has become a serious problem for patients who are already very ill, especially those with weak immune systems, catheters, breathing tubes, or long hospital stays.
Now, scientists in the United Kingdom and the Netherlands have watched the pathogen during infection inside a living host and found a possible weak point. The fungus switches on genes that help it grab iron, a mineral it needs to grow, and that survival trick may also point toward future treatments.
A fungus built for hospitals
Candida auris is a type of yeast, which means it is a fungus, not a bacterium. The CDC says it can cause life-threatening infections and often resists antifungal medicines, the drugs used to treat fungal disease.
The scary part is not only what it does inside the body. It can also live on skin and hospital surfaces, including bedrails, doorknobs, and medical equipment, making it easier to pass from one vulnerable patient to another.
The World Health Organization placed Candida auris on its first fungal priority pathogens list in 2022, a report meant to push more research, surveillance, and public health action. In bloodstream infections, the new study notes an associated mortality rate of about 45 percent, though many patients are already seriously ill when infection appears.
The iron clue
Iron sounds ordinary. It is in our blood, in food, and in many daily health conversations, but for microbes it can be the difference between growing and failing.
Inside the human body, iron is tightly guarded. That is one way the immune system tries to starve invaders, and Candida auris appears to fight back by turning on genes that help it pull in iron-carrying molecules during infection.
Dr. Rhys Farrer, from the University of Exeter’s MRC Center for Medical Mycology, put it plainly. “Until now, we’ve had no idea what genes are active during infection of a living host,” he said, adding that the findings give researchers “a potential target for new and already existing drugs.”
A fish model opened the window
The study was led by Hugh Gifford and co-supervised by Farrer and Tetsuhiro Kudoh, with collaborators including Johanna Rhodes at Radboudumc and Imperial College London. Instead of relying only on mice or zebrafish, the team used Arabian killifish larvae, whose eggs can tolerate human body temperature.
Why does that matter? Because Candida auris is hard to study during active infection, and researchers needed a living model that could show the fungus adapting in real time, almost like watching a quiet break-in through a security camera.
The work was supported by Wellcome, the Medical Research Council, and NC3Rs, the UK organization that promotes replacement, reduction, and refinement in animal research. NC3Rs said the model gave scientists unusual insight into what happens inside live infected hosts.
What the fungus did next
Under the microscope, the team saw that some Candida auris strains could stretch into threadlike filaments. In simple terms, the cells became longer, a shape that may help the fungus search for nutrients and survive under pressure.
The iron finding was broader. Across the five major branches of Candida auris studied, the fungus switched on genes linked to nutrient pumps that can bring iron-related molecules into the cell.
There was also a very practical problem. Farrer told Infobae that the fungus was so sticky during microinjection work that the team had to change its method, a small lab detail that echoes a bigger hospital concern, since Candida auris can cling to plastics, catheters, and surfaces.
A different kind of treatment target
Most people think of treatment as killing a germ outright. But this study points to another route, which is stopping Candida auris from doing the things that make it dangerous.
Dr. Guillermo García Effron, a Conicet researcher and mycology laboratory director at the National University of the Littoral in Argentina, told Infobae that the study helps explain a virulence mechanism, meaning a way the fungus causes disease. He said the idea is not simply to “kill” the microorganism, but to stop it from causing infection.
That distinction matters because fungi and humans both have complex cells, which can make antifungal drug design tricky. García Effron also warned that no advanced antifungal treatment currently blocks this specific virulence mechanism, so the approach remains promising but early.
What comes next
This is not a new treatment yet. The biggest limitation is clear enough for anyone to understand, since the work was done in killifish larvae, not in people, so researchers still need to test whether the same iron-hunting genes switch on during human infection.
Still, the discovery gives scientists a sharper map. Earlier research has already suggested that disrupting iron balance and metabolism may weaken Candida auris, and this new work adds a living-infection view of why that line of attack deserves attention.
For hospitals, the immediate tools remain fast detection, careful screening, strict cleaning, and infection control. For researchers, the next question is more targeted and urgent. Can the fungus be starved of the iron it needs before it does serious damage?
The main study has been published in Communications Biology.
