Candida auris (C. auris) has become a significant challenge in critical care across the country. It spreads across surfaces, equipment, and even skin, allowing outbreaks to take hold long before they are detected. These infections tend to appear in patients with comorbidities like advanced age, diabetes, kidney disease, malignancy, dialysis dependence, immunocompromised states, invasive devices, recent surgery, severe viral illness, and broad-spectrum antimicrobials. These all increase the likelihood that colonization will progress into invasive disease.
C. auris‘ environmental resilience complicates containment and drives transmission. The resistance profile adds another layer of difficulty. Most isolates are resistant to fluconazole, and many are resistant to amphotericin (30% in my patient population). Even with echinocandins as first-line therapy, the risk of failure or relapse is higher than with other Candida species. When there is concern for central nervous system involvement, I sometimes add intravenous liposomal amphotericin, recognizing that resistance remains possible.
Rapid identification is key. Our facility uses the Simplexa C. auris Direct PCR assay targeting the ITS2 gene on axilla and groin swabs. Early recognition guides isolation, environmental cleaning, and timely initiation of echinocandins. Once candidemia is suspected or confirmed, source control becomes just as crucial as antifungal therapy. Removing central lines, reassessing surgical sites, and eliminating any nidus of infection can change the trajectory for critically ill patients.
Despite these efforts, C. auris carries a high mortality rate, often exceeding 50% in international cohorts. These outcomes reflect the severity of illness in affected patients, delayed recognition, and the organism’s resistance patterns. It also stresses the importance of strong infection prevention practices, antimicrobial stewardship, and coordinated efforts across the hospital.
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