COMMENTARY

Candida auris: Time to Prick Up Your Ears?

Paul G. Auwaerter, MD

Disclosures

December 15, 2016

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Hello. This is Paul Auwaerter, speaking for Medscape Infectious Diseases and from Johns Hopkins University School of Medicine.

Candida and antifungal resistance, to me as a nonmycologist, seems relatively static. Azole resistance in Candida albicans infection is relatively uncommon in those who have not been previously heavily exposed to azoles. Candida lusitaniae is resistant to amphotericin. Candida krusei is resistant to fluconazole. Candida glabrata is increasingly resistant to fluconazole, and recently there have been concerns that echinocandin resistance may be increasing.

A report in the November 2016 Morbidity and Mortality Weekly Report (MMWR)[1] highlighted a new species, Candida auris, that had a couple of features that I thought deserved some thoughtful consideration. It was initially described from an external ear drainage in Japan in 2009 (auris means "ear" in Latin). There have been reports, mainly overseas, of this particular pathogen causing 20%-60% mortality and afflicting hosts with significant comorbidities (eg, corticosteroid use, prolonged hospitalizations, antibiotic exposure, and malignancies).

C auris may be misidentified or difficult to identify by conventional systems. It might be identified as an alternative Candida species, such as Candida haemulonii, or even Saccharomyces cerevisiae. We are not exactly sure how common this might be. The Centers for Disease Control and Prevention and the United Kingdom discussed these [concerns] earlier in the spring and summer and asked for reports of any unrecognized Candida isolates.

The MMWR described [the first] seven C auris isolates in the United States. What impressed me from the report and also from some of the existing literature is as follows[1,2,3]:

  • Although the pathogens in the United States were not as resistant to multiple drugs as those described globally, they were resistant to fluconazole. In the global reports, isolates were described as being resistant to amphotericin, echinocandins, and even flucytosine. It looks like this particular species, much like C glabrata, may have increased capabilities of developing resistance, perhaps under pressure of significant antifungal therapies.

  • Not only in this series of seven patients, but also overseas, [these infections] were described through whole-genome sequencing as probably also spreading sometimes clonally within a hospital and infecting other patients. Perhaps this is not a surprise. As this tool is being used more often for molecular identification of outbreaks, we may also be seeing that infections from multiple drug-resistant pathogens are indeed more of a clonal mini-outbreak than separate events.

With C auris, and maybe also with C glabrata, we may be seeing the emergence of a drug-resistant pathogen, perhaps because of our increasing use of antifungal therapies in patients with difficult health problems. This may mean that we now should be on the lookout. In fact, that is the advice for this infection: Consider implementing infection control methodologies to help prevent its spread.

We have thought about methicillin-resistant Staphylococcus aureus, vancomycin-resistant Enterococcus, highly drug-resistant gram-negative [organisms], and tuberculosis, but we now may be entering an era of multiple drug-resistant fungal pathogens where we need to take a similar view. It does not seem to be moving with such dispatch as in the bacterial arena; however, we have to stay tuned. We are not quite sure how common this pathogen is.

I am sure we will learn more in months and years to come. This is perhaps one of the first new fungal resistance forays that is grabbing our attention, and we need to be watching. Thanks for listening.

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