Candida auris is hard to control because it colonizes human skin without symptoms, persists for weeks on hospital surfaces and equipment, resists multiple antifungal drug classes, and is frequently misidentified by routine lab tests. These features enable silent spread in healthcare facilities, delayed effective therapy, and outbreaks that are difficult to stop. Containment requires targeted screening, strict infection prevention, reliable diagnostics, and careful use of limited antifungal options.
What is Candida auris?
Candida auris is a yeast that emerged in 2009 and has since caused healthcare associated outbreaks worldwide. Unlike many other Candida species that live in the gut, C. auris commonly colonizes the skin and the outer ear, and it can cause invasive infections such as bloodstream infections in hospitalized or long term care patients. Public health agencies classify it as an urgent threat because many isolates are resistant to one or more antifungal drug classes (CDC overview) and it spreads efficiently in healthcare settings.
C. auris can colonize patients for months and survive on surfaces for weeks, which supports ongoing transmission in healthcare environments CDC.
How does Candida auris spread and persist in healthcare settings?
Most transmission occurs through contact, especially in hospitals and long term care facilities. C. auris colonizes skin, particularly in moist areas, and sheds onto bed rails, furniture, mobile devices, and shared equipment. The organism forms biofilms and tolerates many commonly used disinfectants, which allows environmental persistence when cleaning is suboptimal. Outbreaks have been linked to gaps in hand hygiene, shared equipment that is not fully decontaminated, and patient transfers between facilities (ECDC), (MMWR 2023).
- Skin colonization without symptoms supports undetected carriage
- Environmental survival for weeks enables indirect transmission
- Biofilms on plastics and devices protect cells from cleaning and drugs
A CDC analysis reported a 95 percent increase in clinical C. auris cases in the United States from 2020 to 2021, underscoring ongoing transmission pressure in healthcare facilities MMWR.
Why is Candida auris resistant and hard to treat?
C. auris shows intrinsic and acquired resistance patterns that are uncommon in related yeasts. Many isolates are resistant to fluconazole, a substantial fraction have elevated minimum inhibitory concentrations to amphotericin B, and echinocandin resistance, while still less common, has been increasing and has caused treatment failures (CDC). Resistance arises through multiple mechanisms, including mutations in drug targets, upregulated efflux pumps that expel drugs, cell wall and membrane adaptations, and stress response pathways that help the fungus survive hostile conditions.
First line therapy for invasive disease is usually an echinocandin, with careful follow up of clinical response and susceptibility results. If resistance or poor response is suspected, combinations or alternative agents may be required in consultation with infectious diseases specialists (IDSA candidiasis guidance). The limited antifungal arsenal means inappropriate initial therapy or delayed active treatment can worsen outcomes.
Why is Candida auris hard to detect quickly?
Standard biochemical identification systems often misidentify C. auris as other yeasts, which delays both targeted treatment and infection control. Accurate detection requires updated MALDI TOF mass spectrometry databases or molecular methods such as PCR, which are not uniformly available in all labs (CDC diagnostics overview), (ECDC laboratory advice). Because asymptomatic colonization is common, facilities also need active screening, for example composite skin swabs, to find carriers during outbreaks or on admission from high risk settings.
Who is at highest risk, and what does this mean for infection prevention?
Serious infections occur primarily in people with risk factors such as prolonged hospitalization, residence in long term care, invasive devices like central lines and ventilators, recent surgeries, broad spectrum antibiotic use, and immunosuppression from conditions or medications. On its own, exposure usually is not enough to cause invasive disease. The danger rises when the immune system is weakened and the healthcare environment allows the organism to persist.
For infection prevention teams, C. auris requires a layered approach that goes beyond standard practices used for other Candida species:
- Rapid identification and isolation or cohorting of colonized and infected patients
- Contact precautions, dedicated equipment, and enhanced environmental cleaning with disinfectants active against C. auris, such as products with EPA List P claims
- Targeted screening of contacts and admissions from high risk facilities
- Communication of C. auris status during patient transfers between facilities
- Antimicrobial stewardship to reduce selection pressure
These steps are detailed in public health guidance for healthcare facilities (CDC infection control) and by European authorities (ECDC).
What does current research say, and what are the limitations?
A 2025 review in Microbiology and Molecular Biology Reviews synthesizes how C. auris persists on skin, withstands disinfectants, evades parts of the immune response, and accumulates multiple resistance mechanisms, helping explain why conventional strategies struggle to contain it (review DOI). New antifungals and diagnostics are in development, but availability is uneven and clinical data remain limited. Key gaps include optimal decolonization strategies, the best use of combination therapy for resistant isolates, and scalable screening approaches during regional outbreaks.
Until those gaps close, the practical reality is that C. auris control hinges on rapid, accurate detection, rigorous infection prevention, and careful antifungal use guided by susceptibility testing.