A research team has identified a mechanism that lets the hospital fungus Candidozyma auris survive treatment with echinocandins, the drugs of first choice against such infections, Tagesspiegel reports. Under drug pressure, the pathogen makes extra copies of its entire genome, raising the chance that changes such as those in a gene called CRZ1 take hold and lead to resistance. The findings were published in the journal Nature Communications.
The work was led by Hugh Gifford of the University of Exeter. Gifford said the fungus is rarely seen in the general population but poses a lethal threat to intensive care patients. It clings to patients' skin and to the equipment around them, can pass from person to person, and is extremely hard to eliminate. Once the infection reaches the bloodstream of a weakened patient, the mortality rate is 45 percent, he said. Outbreaks in intensive care units are also costly for hospitals and cause major disruption.
Why it matters
Echinocandins attack the fungal cell wall and are considered the leading treatment for these infections. Until now, resistance to these drugs was mainly linked to alterations in the genes FKS1 and FKS2. The Exeter team examined why two seriously ill patients failed to recover despite echinocandin treatment, and found no such alterations in either case.
The study also points to resistance developing in stages rather than all at once: greater tolerance first, then further genetic changes, and finally more pronounced resistance. That picture matters for hospitals, where the fungus has been reported in outbreaks on every continent.
An accidental discovery
The clue came partly by chance. According to Tagesspiegel, a researcher left plates containing Candidozyma auris and the antifungal anidulafungin in culture longer than intended. Only then did the team notice that a tiny fraction of cells had kept growing over several days.
Longer cultivation also produced two clearly distinct colony types, a small variant and a large one. The small colonies grew slowly, the large ones quickly. Testing showed the fungus had survived the antifungal by generating additional copies of its whole genome, which increased its chances of mutating in a way that let it escape the drug.
The faster-growing cells from the large colonies carried considerably more mutations in CRZ1 than the original isolates and the small variants did. CRZ1 is associated with the stability and remodeling of the cell wall, and further tests suggested that the cell-wall response of the fast-growing cells to antifungals had changed.
A German perspective on case numbers
Germany is among the EU countries with the most reported cases, according to data from the European Centre for Disease Prevention and Control cited by Tagesspiegel. Oliver Kurzai, head of the Institute for Hygiene and Microbiology at the University of Würzburg and director of the National Reference Centre for Invasive Fungal Infections, said there are currently about 100 initial detections per year, a relatively stable figure. Kurzai was not involved in the British study.
Outbreaks keep occurring, he said, and as the pathogen spreads, especially in southern Europe, the likelihood of more imported cases rises. "We must therefore expect case numbers to increase in the coming years," Kurzai said. Germany now requires that detections be reported. Echinocandin resistance remains rare in the country, appearing in fewer than five percent of confirmed strains.
Candidozyma auris, formerly known as Candida auris, was first described in Japan in 2009, and its origin is still unexplained. Outbreaks have been reported in more than 60 countries, and the World Health Organization lists it among its highest-priority fungal pathogens.
A second fungus draws attention in the US
In the United States, concern is focused on a different dangerous fungus, Cladophialophora bantiana. Infections with it are fatal in 60 to 70 percent of cases, according to the US Centers for Disease Control and Prevention. The number of detections at one clinical reference laboratory rose roughly fourfold between 2023 and 2025, albeit from a low level, and the CDC says the reasons for the apparent increase are unknown.
Such molds typically cause brain abscesses, according to the Robert Koch Institute, and infections occur worldwide, mostly in people over 50. Kurzai said cases in Germany remain a rarity, and no systematic recording exists.
Possible causes for rising fungal infection numbers vary, Tagesspiegel reports. Better diagnostics play a role. A link to climate change is considered plausible, particularly warming and long periods of drought, since spores can travel through the air with dust and soil. So far this remains a hypothesis without direct proof.
What to watch
Gifford and his colleagues say their discovery means new ways must be found to treat patients and rid hospitals of the fungus. They now plan to examine options including combining different antifungals.
