There's a new fungus amongus, and it's raising red flags among health care experts because it resists all the major antifungal treatments.
The discovery involves Candidozyma auris (formerly known as Candida auris), an emerging fungal pathogen that has already become a serious problem in hospitals around the world.
Since it was first described in 2009, this fungus has spread to more than 60 countries across six continents, causing healthcare-associated outbreaks and invasive infections, with mortality rates of 30–50 percent reported in some situations.
The fungus can persist in healthcare environments and spread easily between patients. Because of its combination of antifungal resistance and potential for wider spread, the World Health Organization designated C. auris a critical-priority fungal pathogen in 2022.
But the particular strain of this fungus described in a new paper has something especially troubling going for it: laboratory testing found it resistant to all four major classes of antifungal drugs.
The isolate was recovered from a 28-year-old woman who developed a hospital-acquired surgical-site infection after elective surgery at a hospital in Nairobi, Kenya. It's the first such case in Africa.
The woman's wound swab eventually grew C. auris, and genomic testing confirmed that the fungus belonged to one of the clades associated with high levels of antifungal resistance.
The researchers call this particular strain pan-drug-resistant, or PDR–meaning it was resistant to the antifungals in familiar drugs like fluconazole, caspofungin, micafungin, amphotericin B, and flucytosine.
Pan-drug resistance like this is exceptionally rare. The researchers describe their Kenyan isolate as the first PDR C. auris identified in Africa and only the second globally documented case; another had previously been reported in New York in 2022.
To better understand this resistance, the team sequenced its entire genome.
They found several mutations already associated with antifungal resistance, including changes in the genes ERG11 and CDR1, which are linked to resistance to azole drugs, an alteration in the FKS1 gene associated with resistance to echinocandins, and a "stop-gain" mutation in FUR1, a gene involved in processing the drug flucytosine.
The strain's genetic profile may provide clues about how its resistance arose.
The researchers note that the mutations differ from those found in previously reported strains in New York, raising the possibility that pan-drug resistance evolved independently rather than simply being imported from the United States to Kenya.
But it is still possible.
Nor can they determine whether the patient's previous exposure to antifungal drugs helped select for resistance. Her clinical history shows that she received several antifungal medications during her illness, but the researchers didn't have enough information about doses and treatment durations to establish whether those drugs drove the evolution of resistance in this particular infection.
The authors call this finding alarming, especially in regions where access to newer antifungal drugs can be limited.
The authors point to the "escalating threat of untreatable fungal infections" and call for stronger surveillance of fungal genomes, as well as "rapid diagnostic capacity to mitigate the spread of highly resistant C. auris lineages in healthcare settings," as they write in the paper.
For now, the highly resistant C. auris is super-rare. But it has already demonstrated its ability to move through hospitals, acquire resistance, and evolve in response to treatment.
A fungus that can survive nearly every standard antifungal weapon is a reminder that, in the microbial arms race, the enemy doesn't have to be common to be consequential.
The research has been published in Scientific Reports.
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