A multidisciplinary team of researchers at the University of Wisconsin–Madison has identified a promising new therapeutic candidate against Candida auris, an emerging fungal pathogen able to resist multiple antifungal drugs and spread rapidly through hospitals and care facilities. Supported by funding from the National Institutes of Health, Dr. Jeniel Nett, an associate professor of medicine at the UW School of Medicine and Public Health, led a team that studied the yeast for weaknesses that could be exploited in the fight against it. The need is urgent; certain strains of Candida auris are resistant to all three of the major classes of antifungal drugs. Between 30% and 60% of patients who develop a Candida auris infection die, usually from sepsis after the fungus enters their bloodstream.
Nett and her colleagues identified potassium as essential to Candida auris’ growth on skin. They also discovered that eliminating a single Candida auris gene, TRK1, was enough to stop the fungus from growing. The gene encodes a protein by the same name that transports the potassium required for Candida auris to grow and colonize on skin and other surfaces. Researchers believe that the transporter’s distinctive structure could make it a potential target for drugs to disrupt colonization on skin. Because humans lack the TRK1 protein, a drug that targets it is less likely to harm human cells.
