New clues to how infectious fungus Candida auris resists antifungals

The fungus Candida auris has spread to more than 60 countries. It’s a growing concern because it can cause serious infections in already hospitalized patients. Now, researchers at the University of Exeter and City St George’s, University of London, have discovered mechanisms that help explain how the fungus survives certain antifungal treatments. The findings could help guide the development of new strategies to combat this pathogen.

The researchers published their peer-reviewed study in the journal Nature Communications on October 15, 2026.

A fungus that is difficult to eliminate

First identified in 2008, Candida auris has become a global public health concern. It can live on the skin and persist on surfaces and medical equipment, making it easier to spread in hospitals. Those most at risk are people who are already seriously ill, particularly patients in intensive care units. If the fungus enters the bloodstream, the infection can be fatal.

But controlling it is not always easy. Some infections persist despite treatment, even when initial laboratory tests suggest that the fungus should respond to the medication.

To understand why this happens, the researchers studied how Candida auris responds to echinocandins, a class of antifungal drugs used to treat serious infections. These drugs work by weakening the fungal cell wall.

Fungus Candida auris changes its cell wall to resist treatment

During one experiment, a researcher accidentally left some samples incubating longer than intended. When the researcher returned to examine them, they found something unexpected: some cells had survived the treatment and started growing again.

One mechanism that could explain how these cells survived involves the cell wall, the structure that protects the fungus. Echinocandins work by blocking an enzyme the fungus needs to produce beta-glucan, one of the main components of its cell wall. By interfering with its production, the drugs weaken the structure that protects the cells.

However, the researchers observed that Candida auris responded by changing the composition of its cell wall. The fungus increased the amount of chitin, another component of the wall, and thickened its inner layer.

By increasing chitin levels and thickening this inner layer, the fungus may be able to compensate for some of the weakening caused by the disruption of beta-glucan production.

Genetic changes help the fungus adapt

In addition to modifying its cell wall, the researchers discovered that Candida auris had extra copies of certain sections of its genetic material. Having multiple copies may allow changes to occur in one of them. If one of these changes helps the fungus resist the antifungal drug, the cells carrying it may be more likely to survive and multiply.

To better understand how these findings relate to drug resistance, the researchers compared the cells that had survived treatment. They found that some formed small colonies and grew slowly, while others formed larger colonies and grew more quickly.

Different populations respond differently to treatment

Although both populations showed resistance to the antifungal drug and shared changes in their cell walls, the researchers found differences in their genetic material.

The cells that formed larger colonies and grew faster had accumulated more changes in a gene involved in the stress response and the maintenance of the cell wall. These changes were associated with even greater resistance to the antifungal drug.

The findings suggest a possible progression: changes in the cell wall may help the fungus withstand the initial effects of treatment, while the accumulation of certain genetic changes may contribute to the emergence of cells that can resist the drug more effectively and grow faster.

New clues for fighting the fungus Candida auris

Although Candida auris remains a significant challenge, learning more about how it resists antifungal drugs is an important step toward combating it. These findings open up new avenues for research and could help guide the development of more effective treatments.

The research team is already investigating combinations of antifungal drugs in the hope of using this knowledge to find new ways to fight the fungus.

Bottom line: Scientists have identified new resistance mechanisms used by the fungus Candida auris, paving the way for advances in antifungal treatments.

Source: FKS1/2-variant independent mechanisms underlying the emergence of resistance in echinocandin-refractory Candida auris infections.

Via University of Exeter

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