Candida auris is an emerging yeast that presents a severe threat to patients in healthcare settings worldwide. This fungus is a type of yeast that can cause serious illnesses, ranging from wound and ear infections to life-threatening bloodstream infections, particularly in individuals with compromised immune systems. It is an urgent concern because it is highly transmissible within hospitals and long-term care facilities. The threat is compounded by the fact that C. auris is often resistant to multiple types of antifungal medications, making infections difficult to treat effectively.
The Challenge of Fungal Resistance
The primary reason C. auris is difficult to kill lies in its inherent drug resistance and its ability to survive in both the human body and the external environment. Many strains are multidrug-resistant, meaning they are not killed by at least two of the three main classes of antifungal drugs. Nearly all isolates show resistance to the triazole drug fluconazole, a common first-line treatment for other fungal infections.
Resistance often results from genetic mutations or the presence of efflux pumps, specialized proteins that actively pump antifungal drugs out of the fungal cell before they can cause damage. Upregulation of efflux pumps, such as MDR1 and CDR1, increases the fungus’s tolerance to azole drugs. This ability to neutralize common medications challenges clinicians attempting to manage an active infection.
A further complication is the organism’s capacity to form biofilms, dense communities of cells encased in a protective matrix. This structure acts as a physical shield, making the fungal cells substantially more tolerant to antifungals than free-floating cells. The concentrations of echinocandins needed to inhibit C. auris biofilms can be far higher than the levels safely administered to a patient.
The extracellular matrix contains mannan-glucan complexes, polysaccharides that physically sequester antifungal drugs, preventing them from reaching cellular targets. Biofilm formation is instrumental in the fungus’s persistence in the healthcare environment, allowing it to survive on surfaces like plastic and metal for prolonged periods, sometimes up to four weeks. This persistence requires specialized, high-potency methods for both clinical and environmental eradication.
Clinical Treatment of Infection
When an active, invasive C. auris infection is confirmed, the primary pharmacological strategy relies on the echinocandin class of antifungal drugs. Echinocandins (anidulafungin, caspofungin, and micafungin) are recommended as the initial therapy for adults and children over two months old because most strains remain susceptible. These drugs inhibit beta-1,3-D-glucan synthase, an enzyme necessary for building the fungal cell wall, ultimately leading to cell death.
Treatment requires careful monitoring and is only recommended for patients showing signs of an active clinical infection. Patients who are merely colonized—meaning the yeast is present without causing disease—are not treated with antifungals, as this practice can drive further resistance. Antifungal susceptibility testing is performed on clinical isolates to confirm the strain’s resistance profile and guide therapeutic decisions.
If the infection is resistant to echinocandins, or if the patient fails to improve after five days, therapy shifts to liposomal amphotericin B. This polyene drug binds to ergosterol in the fungal cell membrane, disrupting its integrity. In cases of pan-resistance—resistance to all three major classes of antifungals—or treatment failure, physicians may consider combination therapy, such as an echinocandin combined with liposomal amphotericin B, though evidence is limited.
Infants under two months old are an exception, with amphotericin B deoxycholate being the initial recommended treatment. Given the complexity of resistance patterns, consultation with an infectious disease specialist is considered for all suspected or confirmed cases to ensure appropriate drug selection and dosing. Treatment is often a dynamic process, adjusting based on the patient’s response and the specific characteristics of the infecting strain.
Environmental Eradication Methods
Killing C. auris in the healthcare environment requires specific, high-level disinfectants because the fungus persists on surfaces for long periods and is not eliminated by commonly used cleaning agents. Disinfectants based on quaternary ammonium compounds (QACs) are ineffective, necessitating the use of sporicidal-level agents. The Environmental Protection Agency (EPA) maintains List P, a list of approved products that have demonstrated efficacy against C. auris.
Successful environmental eradication relies on disinfectants containing active ingredients such as sodium hypochlorite (bleach), hydrogen peroxide, or peracetic acid. Sodium hypochlorite is used at 1000 parts per million (ppm) of available chlorine for terminal cleaning, performed after a patient is discharged or transferred. Proper application and ensuring the correct contact time are necessary for successful environmental elimination.
No-touch technologies are integrated into the cleaning process as a supplemental measure to reach surfaces manual cleaning might miss. Vaporized hydrogen peroxide (VHP) is one such method, used successfully to control outbreaks. While UV-C light has germicidal effects, C. auris shows less susceptibility to it compared to other pathogens, meaning it is best used as an adjunct rather than a standalone solution.
Infection Control and Prevention
Preventing the spread of C. auris within healthcare facilities is the most effective way to minimize the threat. Strict adherence to hand hygiene protocols by all healthcare personnel is foundational; alcohol-based hand rubs are effective and preferred when hands are not visibly soiled. When hands are visibly soiled, they must be washed with soap and water.
Patients known to be infected or colonized are immediately placed on transmission-based precautions, typically involving housing them in a single-occupancy room. Healthcare workers must use personal protective equipment (PPE), specifically gloves and gowns, when entering the patient’s room and remove them carefully before leaving. This practice minimizes the transfer of the yeast from the patient’s skin or contaminated surfaces onto the worker’s clothing or hands.
Meticulous cleaning and disinfection of all shared medical equipment, such as glucometers and blood pressure cuffs, after each use is necessary for control. Facilities implement screening programs to identify colonized patients, especially those at high risk or those who had close contact with a known case. Identifying colonization triggers enhanced infection control measures, which is paramount to containing the spread of this persistent fungal pathogen.