Essential reading on Candida auris

During my intern rotation on the University of Virginia bone marrow transplant unit, I convinced myself that a Candida krusei epidemic was brewing. One of my patients was infected, and the bug was (and is inherently) resistant to fluconazole, a drug that had only recently been introduced (yes, I’m old—the year was 1990). This never really came to pass—despite 30 years of widespread fluconazole use, C. krusei still accounts for < 5% of invasive candidiasis, and outbreaks are rare. 

Now, a Candida species that wasn’t even described a decade ago is emerging as a major problem in ICUs around the world. The Candida auris story is fascinating, puzzling, and concerning. For reasons nobody understands, the species emerged (or began to recognized) almost simultaneously on three different continents. Although risk factors for invasive C. auris are similar to those for other causes of invasive candidiasis (ICU stay, antibiotic exposure, device use), it also features high rates of antifungal resistance, persistence on environmental surfaces, resistance to commonly used disinfectants, frequent transmission in ICU environments, and has thus caused several large, difficult-to-control outbreaks.

If you want to catch up on this emerging pathogen without spending hours on a literature review, there’s an excellent summary publication now out in Clinical Microbiology Reviews from Anna Jeffery-Smith and colleagues. See Table 4 for a summary of infection prevention recommendations from UK, US, EU and South Africa.

Lab capacity and emerging infections

Question: What do mcr-1 and Candida auris have in common?

Answer: Both are emerging infection threats, and neither can be identified by most hospital laboratories. 

The mcr-1 gene, which confers resistance to colistin and can be plasmid-mediated (and thus easily spread), was first described in November of 2015 but is now known to be present in over 20 countries (it has also been found in archived organisms going back over 30 years). Of course, it didn’t just suddenly appear everywhere at once—it has been spreading for a long time undetected, and will continue to do so. Many laboratories don’t test for colistin susceptibility, and such testing is highly problematic—the properties of the compound interfere with diffusion through agar and cause adherence to the surfaces used for broth dilution trays (resulting in variable performance by test method). There isn’t even agreement on the breakpoint for resistance. Thus those labs that do perform testing only do so on multiple-drug resistant organisms or upon request—and if resistance is detected, the organism must be sent to a reference lab for molecular detection of the gene (CDC recommends sending Enterobacteriaceae with colistin MIC of 4 mcg/mL or higher, unless they are Proteus, Providencia, Morganella, or Serratia, which have intrinsic colistin resistance).

Candida auris is another interesting story. First described in 2009 in the external ear canal of a patient in Japan, C auris has now been detected in 9 different countries, can cause invasive candidiasis in hospitalized patients, has outbreak potential, and can be resistant to all three major antifungal classes. But again, conventional methods for fungal identification do not identify this newer species (biochemical panels most often ID it as C. haemulonii), and many labs never go beyond the “big 5” species (albicans, glabrata, parapsilosis, tropicalis and krusei), calling the rest “other Candida spp”. MALDI-TOF may soon be useful, but for now it is best to look more closely at invasive yeast isolates that ID as related species (e.g. haemulonii) or that are unusually resistant (provided your lab does antifungal susceptibility testing routinely on invasive isolates). 

These two emerging threats reinforce the importance of investment in lab capacity at all levels, from the individual hospital to state, regional and national public health laboratories.

Now to celebrate the 4th of July weekend, a submission from the 2015 ASM Agar Art Challenge: