Candida auris gains drug resistance through changing genome copies
A single peer-reviewed investigation followed Candida auris from two patients whose infections persisted despite antifungal treatment. Rare cells tolerated high drug concentrations without familiar resistance mutations. Laboratory experiments linked adaptation to increased genome copies and altered cell walls. The small clinical sample describes one route toward resistance and leaves its frequency among patients unresolved.
Science··Evening
Persistent infections lacked familiar mutations
Candida auris, a fungus found in bloodstream infections, persisted or returned in two intensive-care patients in London despite anidulafungin treatment. A single peer-reviewed investigation followed their isolates using genome sequencing and susceptibility experiments. The samples lacked the expected protein-altering variants of FKS1 or FKS2, the genes encoding the target of this antifungal. The two hospitals were St George’s and King’s College in London.[1]
Rare cells survived concentrations that suppressed the majority
Small subpopulations grew at drug concentrations that suppressed most cells, a pattern called heteroresistance. Under laboratory drug pressure, small and large colony variants appeared with increased DNA content and changes in cell-wall composition. Some cells carried additional copies of their genome. Removal of drug pressure could reverse those changes. Faster-growing large colonies also showed more mutations in CRZ1, a gene involved in the stress response.[1]
Laboratory adaptation followed a stepwise course
The researchers interpret the findings as physiological adaptation that can precede the selection of more stable genetic resistance. Routine susceptibility measurements can miss rare resistant subpopulations. The clinical evidence covers two patients and cannot establish how common this route is. Both patients later died, although neither death was directly attributed to the fungal bloodstream infection. The work investigates resistance mechanisms rather than testing a new medicine’s efficacy.[1]
