Scientists uncover how Candida auris resists antifungal drugs

Researchers identify cell wall changes and genetic amplification behind treatment failure

By LineZotpaper

Published20 October 2026

Read Time2 min

Researchers at the University of Exeter and City St George's, University of London have discovered mechanisms that help explain how the infectious fungus Candida auris survives certain antifungal treatments, according to a study published October 15 in Nature Communications.

The fungus Candida auris, first identified in 2008, has spread to more than 60 countries and poses a growing public health threat, particularly to hospitalized patients in intensive care units. It can live on skin and persist on surfaces and medical equipment, making it difficult to control in healthcare settings.

In the study, researchers investigated how the fungus responds to echinocandins, a class of antifungal drugs that work by weakening the fungal cell wall. The team observed that Candida auris can survive treatment by altering its cell wall composition. The fungus increased the amount of chitin, another component of the wall, and thickened its inner layer. This may compensate for the weakening caused by the disruption of beta-glucan production, which echinocandins target.

Additionally, the researchers discovered that the fungus had extra copies of certain sections of its genetic material. Having multiple copies may allow changes to occur in one copy; if a change helps resist the antifungal drug, cells carrying it may survive and multiply.

When comparing cells that survived treatment, the researchers found two distinct populations: some formed small colonies and grew slowly, while others formed larger colonies and grew more quickly. Both showed resistance to the drug and shared cell wall changes, but the faster-growing population had accumulated more changes in a gene involved in stress response and cell wall maintenance, associated with even greater resistance.

The findings suggest a progression where cell wall changes help the fungus withstand initial treatment, while genetic changes contribute to the emergence of more resistant, faster-growing cells.

The research team is now investigating combinations of antifungal drugs to find new ways to fight the fungus.

Analysis

Why This Matters

Candida auris causes serious, sometimes fatal infections in already vulnerable patients, and its resistance to treatment makes it harder to manage in hospitals.
Understanding the mechanisms of resistance could guide development of more effective antifungal strategies, potentially saving lives.
The fungus's ability to persist on surfaces and medical equipment means outbreaks can be difficult to contain, amplifying the need for new treatments.

Background

Candida auris was first identified in 2008 and has since become a global health concern, spreading to over 60 countries. It is particularly dangerous for people who are already seriously ill, such as patients in intensive care units. If it enters the bloodstream, the infection can be fatal. Echinocandins are a key class of antifungal drugs used to treat such infections, but some infections persist despite treatment, even when laboratory tests suggest the fungus should respond.

Key Perspectives

Researchers (University of Exeter and City St George's, University of London): The study provides new insights into how Candida auris adapts to antifungal drugs, showing that both cell wall changes and genetic amplification play roles in resistance. The team is now exploring combination therapies. Healthcare professionals: For clinicians treating patients with Candida auris infections, understanding why treatment sometimes fails could inform better patient management and infection control practices. Public health experts: The spread of a drug-resistant fungus in hospital settings is a growing concern, and research like this is critical for developing strategies to prevent and control outbreaks.

What to Watch

Results of ongoing research into combination antifungal therapies that might overcome the resistance mechanisms identified.
Whether similar resistance mechanisms appear in other fungal pathogens.
Updates on the global spread of Candida auris and reports of treatment failures in clinical settings.

Sources

New clues to how infectious fungus Candida auris resists antifungals · EarthSky

Checked

12 claims in this story checked against 1 source: 10 supported.

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Partly supportedScientists have uncovered how Candida auris resists antifungal drugs.EarthSky: “new research is helping to uncover how it resists antifungal drugs”
Partly supportedCell wall changes and genetic amplification are behind treatment failure.EarthSky: “One mechanism that could explain how these cells survived involves the cell wall”
SupportedResearchers at the University of Exeter and City St George’s, University of London discovered mechanisms that help explain how the fungus survives certain antifungal treatments.EarthSky: “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.”
SupportedThe study was published in Nature Communications on October 15, 2026.EarthSky: “The researchers published their peer-reviewed study in the journal Nature Communications on October 15, 2026.”
SupportedCandida auris has spread to more than 60 countries.EarthSky: “The fungus Candida auris has spread to more than 60 countries.”
SupportedThe fungus poses a growing public health threat, particularly to hospitalized patients in intensive care units.EarthSky: “Those most at risk are people who are already seriously ill, particularly patients in intensive care units.”
SupportedCandida auris can live on skin and persist on surfaces and medical equipment.EarthSky: “It can live on the skin and persist on surfaces and medical equipment, making it easier to spread in hospitals.”
SupportedEchinocandins weaken the fungal cell wall by disrupting beta-glucan production.EarthSky: “Echinocandins work by blocking an enzyme the fungus needs to produce beta-glucan, one of the main components of its cell wall.”
SupportedThe fungus increased its chitin and thickened its inner cell-wall layer.EarthSky: “The fungus increased the amount of chitin, another component of the wall, and thickened its inner layer.”
SupportedCandida auris had extra copies of certain sections of its genetic material, which may allow changes that help cells survive and multiply.EarthSky: “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.”
SupportedSurviving cells formed two groups: some grew slowly in small colonies, while others grew faster in larger colonies.EarthSky: “some formed small colonies and grew slowly, while others formed larger colonies and grew more quickly.”
SupportedThe faster-growing cells had more changes in a stress-response and cell-wall-maintenance gene, associated with greater resistance.EarthSky: “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.”