Useful Candida auris review just published in NEJM. Well worth a read. Here are some brief highlights and points for discussion.

• Candida auris was first identified in 2009, in an isolate from the ear canal of a patient in Japan (“auris” is the Latin word for “ear”). So I tend to say “our-iss”, since the origin of C. auris is the aural canal (and not the oral canal). This feels like a losing battle since most people say “orr-iss”!
• C. auris thrives in high-salt and high-temperature conditions in contrast to other Candida species. This may explain when it can survive in the inanimate environment. It may also explain why it is a globally emerging pathogen linked to climate change. Another aspect of this property of C. auris is the potential for this to explain why it is able to overcome the “endothermy barrier” and cause colonisation / infection in humans. (The high body temperature of endotherms creates a thermal barrier that prevents most fungi from growing in or on them.)
• In the laboratory, C. auris can be misidentified as other candida species. MALDI-TOF is the gold standard for identification. Related to this, many Candida sp. will not be speciated beyond “Candida sp.”. Your lab will be identifying many other Candida species from various anatomical sites (e.g. vaginal swabs). So it could be that C. auris is masquerading as “Candida sp.”
• C. auris is broken down into five clades, I-V. These clades have distinct virulence properties, clinical features, and drug-resistance profiles: the South Asian clade (I), East Asian clade (II), African clade (III), South American clade (IV), and a more recently reported Iranian clade (V).
• C. auris is very able to colonise things – human skin and surfaces of medical devices and other surfaces. The capacity to form biofilms is likely to underpin this ability. Consequently, widespread contamination of the healthcare environment has been reported. Skin colonisation is more common for C. auris than for other Candida species, which are more commonly linked to gastrointestinal colonisation. Prior skin colonisation is associated with subsequent infection. For example, candidemia has developed in up to 25% of critically ill persons who are colonised.
• Risk factors for colonisation or infection with C. auris are similar to antibiotic resistant bacteria such as CPE: age, devices/ventilation, underlying medical conditions, surgical interventions, medicines (including antimicrobial agents and steroids).
• Most strains of C. auris are resistant to fluconazole, and some strains are resistant to all available classes of antifungal drugs. Antifungal resistance varies by clade – some can be virtually pan resistant to antifungal agents. Echinocandins are the treatment of choice for patients with invasive C. auris infection, but are not always especially effective.
• C. auris has spread globally, affecting at least 45 countries. There have been substantial increases in the US in recent years, especially in long-term acute care facilities.
• C. auris candidaemia and invasive candidiasis can be life-threatening, with crude mortality in the 30-60% bracket but it’s difficult to determine attributable mortality.
• From an IPC viewpoint, rapid identification combined with timely application of IPC measures is the cornerstone of prevention.

It seems that C. auris prevalence in the UK is low currently. So let’s do our level best to keep it that way!