From the page · 15 passages with claims
edited by Gaby Clark, reviewed by Robert Egan (Not auto-checked, claim 2)
New research has revealed an unexpected new mechanism through which the killer fungus Candida auris is resisting antifungal drug treatment. (Unverified, claim 3) A team led by the University of Exeter and City St George's, University of London, discovered that the fungus creates multiple versions of its entire genome, including mutating a gene that plays a role in cell wall integrity, called "Crazy-one" (CRZ1). (Unverified, claim 4)
Candida auris was only described for the first time in 2008, and its origins remain a mystery. (2 claims: 2 Unverified) Since it emerged, outbreaks have been reported on every continent, in more than 60 countries in total, including the U.K. It has been named a global public health threat and is on the World Health Organization's critical priority fungal pathogens list. (2 claims: 1 Corroborated, 1 Unverified)
Study first author Dr. Hugh Gifford, clinical lecturer at the University of Exeter's MRC Centre for Medical Mycology, is also an intensive care physician. (3 claims: 3 Not auto-checked) He said, "Candida auris is rare in the general population, but it's a deadly threat to patients in intensive care units. (Unverified, claim 14) It clings to patient skin and surrounding equipment and can be transmitted from person to person—it's incredibly hard to eradicate. (Unverified, claim 15) If infection enters a vulnerable patient's bloodstream, there is a 45% death rate. (Unverified, claim 16)
"Outbreaks in intensive care units have been costly and highly disruptive. (Unverified, claim 17) One unit in the U.K. had to close and undergo complete refurbishment to stop the outbreak, while another outbreak was estimated to cost £1 million to control." (Unverified, claim 18)
An accidental discovery of drug survival (Unverified, claim 19)
The research team was initially testing for drug resistance when a researcher accidentally left plates of cells incubating for longer than the required test period. (Unverified, claim 20) The researcher returned to find that cells had unexpectedly grown during this additional time period. (Unverified, claim 21) They were surprised to find that further testing showed the deadly fungus had survived antifungal treatment by creating multiple versions of its own genome, thereby increasing its chances of mutating to evade the drug and survive. (Unverified, claim 22)
Dr. Sarah Murphy, former postdoctoral researcher at City St George's University of London and co-first author, said, "We initially set out to investigate why antifungal drugs weren't working to kill Candida auris, despite laboratory tests showing that they were not resistant and that the drugs should have been effective. (Not auto-checked, claim 23) We were surprised to discover an entirely new mechanism for this fungus to survive—particularly with luck playing a big part in the discovery. (Unverified, claim 24)
"We tested the fungus against very high concentrations of antifungal drugs. We were amazed to find there was a tiny population of cells that appeared over several days and continued to grow. (Unverified, claim 25) Our discovery means we need to now look at new ways of treating people and eradicating this deadly fungus from hospitals."
Expanding further on the finding, Gifford said, "This study had a number of surprising elements. First, we did not identify any of the DNA mutations that we might have expected. (Unverified, claim 26) Antifungal drugs target the enzymes that make cell walls, so that fungi die by shriveling, exploding or not being able to grow. (Unverified, claim 27) Somehow, these fungi had survived antifungal drugs, and we needed to find out why.
"We were surprised to find that surviving cells had made multiple copies of their entire genome. (Unverified, claim 28) This is a trick that other fungi have used in the past, but not one that is well known in C. auris. (Unverified, claim 29) In fact, there were two populations, some growing slowly, others growing more rapidly. (Unverified, claim 30) We call it 'bet-hedging' when a bug uses multiple tactics to increase its chances of developing resistance and evading treatment."
The team found that the more rapidly growing cells contained a wide range of mutations in a gene that has been studied in other organisms for its role in governing cell wall synthesis, called "Crazy-one" (CRZ1). (Unverified, claim 31) Further tests confirmed the rapid growth of CRZ1 mutants and that their cell walls appeared to be unaffected by antifungal drugs. (Unverified, claim 32)
No passage has a claim with this status.
- Corroborated backed by sources
- Contradicted contradicted by sources
- Unverified not confirmed or contradicted
- Not auto-checked evidence only, no automated status