Plate Nº 90 · recorded October 20, 2026
Health & Medicine ResearchReported finding
Candida auris thickens its wall during antifungal treatment
A study published October 15, 2026, links thicker cell walls, extra gene copies and stress-response changes to survival of Candida auris during echinocandin treatment.
By Marcus Bennett4 min read788 words
In brief
- The peer-reviewed paper appeared in Nature Communications on October 15, 2026.
- C. auris has spread to more than 60 countries and was first identified in 2008.
- Surviving cells increased chitin and thickened the inner cell-wall layer.
- Some survivors carried extra copies of sections of genetic material.
- Fast-growing survivors had more changes in a gene tied to stress response and wall maintenance.
By Marcus Bennett
Candida auris has spread to more than 60 countries, and a study published October 15, 2026, found thicker cell walls and genetic changes in cells that survived antifungal treatment.
The University of Exeter and City St George’s, University of London, published the peer-reviewed study in Nature Communications. The team examined responses to echinocandins, a drug class used for serious infections that weakens the fungal cell wall. Some C. auris infections persist even when initial laboratory results suggest the fungus should respond.
First identified in 2008, C. auris can live on skin and persist on surfaces and medical equipment. Seriously ill patients, especially those in intensive care, face the greatest risk. A bloodstream infection can prove fatal.
What did the researchers find?
The key observation came after a researcher accidentally left samples in growth conditions longer than intended. Some treated cells remained alive and resumed growth after the researcher returned. The team then investigated why these cells persisted.
The survivors showed several traits:
- They increased chitin, a structural carbohydrate in fungal cell walls, and thickened the wall’s inner layer.
- Some carried extra copies of certain sections of genetic material. Those copies may let a useful genetic change arise in one copy.
- The survivors included small, slow-growing cell clusters and larger, fast-growing colonies. Both groups resisted the drug and shared cell-wall changes.
- Fast-growing cells accumulated more changes in a gene involved in the cell’s stress response, or ability to handle damage, and wall maintenance. The researchers associated those changes with even greater resistance.
The authors propose one possible progression. Wall changes may help cells withstand the initial drug effect, while later genetic changes may support stronger resistance and faster growth. The experiment did not show that every survivor passed through both stages.
Takeaway: The fungus appears to reinforce its wall while drugs disrupt a key building block, possibly preserving part of its strength.
How does changing the wall help?
Echinocandins block an enzyme that C. auris needs to make beta-glucan, a major structural sugar in its cell wall. Disrupting beta-glucan production weakens the layer that protects the fungal cell.
The fungus appears to counter some of that damage by increasing chitin and thickening its inner wall. This adjustment may compensate for part of the weakening caused by the drug.
The observations help explain why a laboratory result suggesting that a drug should work may not always match a persistent infection. They do not show that every C. auris population responds in the same way.
Takeaway: Reinforcing the inner wall may provide a partial defense rather than complete protection from echinocandins.
Why can extra gene copies matter?
Extra copies of genetic material can give a fungus multiple versions of the same information. A change in one copy may improve survival without altering the others.
If that change reduces the drug’s effect, cells carrying it may live and multiply more often. That process can increase the share of resistant cells, although the study describes only a possible route.
The fast-growing survivors had more changes in the gene tied to stress response and wall maintenance. Their stronger resistance appeared alongside those changes, so the result supports an association rather than proving every change caused resistance.
Takeaway: Useful changes may gain a survival advantage when gene copies and cell-wall defenses work together.
What could this mean for treatment?
These results give drug developers two concrete research leads: the wall changes that follow echinocandin exposure and the genetic changes associated with stronger resistance. The study did not test a treatment against either target.
The team is already investigating combinations of antifungal drugs. Researchers hope the new mechanisms will guide more effective treatments, but the report gives no successful combination or clinical outcome.
For clinicians, the immediate implication is caution, not a new prescribing rule. A susceptibility test may suggest that a drug should work, yet the experiment offers a biological reason to investigate persistent infection.
Takeaway: Combination therapy is the next research step, not an established solution from this study alone.
What remains uncertain?
The findings come from laboratory cells, including samples that stayed in growth conditions longer than planned. Researchers still need to test how often the same wall and genetic changes arise during routine treatment.
The report does not provide patient counts, resistance frequency, drug doses, or results from a combination trial. It also does not separate every genetic change from every wall change, so the observations cannot yet define a single resistance pathway.
Until clinical studies test the proposed combinations, this work explains a plausible survival route without showing how to defeat it in patients.
Takeaway: The mechanism can guide experiments, but clinical benefit remains unproven.
via nature.com (Original)
More from Marcus Bennett
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News editor covering regulation, policy and their impact on general science news at SciBeat.
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