Researchers have found that multidrug-resistant Candida auris, though capable of forming a biofilm that aids in its spread throughout hospitals, is susceptible to chlorhexidine.
Candida auris, a highly-virulent multidrug-resistant yeast first detected in 2009, has been found to be resistant to antifungals that are effective against its counterparts, capable of forming a troubling biofilm that aids in its spread throughout hospitals, and susceptible to chlorohexidine in a new study conducted by a team of researchers from the Universities of Glasgow and Manchester, University Hospital of South Manchester, and Public Health England.
Leighann Sherry, PhD, a medical mycologist at the University of Glasgow and lead author on the study, warned that the results of the examination of C. auris “suggest it is improbable that the spread and prevalence of C. auris can be controlled with antifungal stewardship alone.” The yeast was first reported in the United States in May 2013 and was the topic of a CDC clinical alert mid-2016.
Due to the fact that the mode of transmission of C. auris is not fully known, the scientists speculated that the pathogen’s ability to form a biofilm could be contributing to its ability to contaminate and colonize patients’ rooms and spread throughout hospitals. Yeasts that are able to form a biofilm can grow on surfaces that otherwise would remain sterile and would not support planktonic, or freely-suspended, cell growth. In addition to comparing the ability of C. auris to form biofilms to C. albicans and C. glabrata, the group also performed antifungal susceptibility testing on both aggregative and nonaggregative strains of C. auris. The scientists also compared the pathogenicity of C. auris and C. glabrata to that of C. albicans by exposing Galleria mellonella larvae to both types of infection.
The research team discovered that C. auris not only forms biofilms, but it does so in “significantly greater volumes” than C. glabrata, although in much smaller quantities than C. albicans. C. auris not only showed predominantly budding yeast when examined via electron microscopy, but also “the occasional pseudohyphae,” the team noted. This biofilm formation is likely key to understanding how and why C. auris spreads through hospital environments and has caused multiple hospital outbreaks in Asia and South America as well as in one UK intensive care unit.
Adding to complications when it comes to spread of the infection, the team discovered that C. auris is not susceptible to the antifungal caspofungin, which has historically been highly effective against Candida biofilms. In fact, C. auris resisted fluconazole, voriconazole, caspofungin, and liposomal amphotericin B. The yeast showed some susceptibility to micafungin and amphotericin B, but the C. auris biofilm resisted these as well except at relatively high concentrations. Chlorohexidine, however, effectively inhibited planktonic and sessile cells in all strains at levels of concentrations typically used for skin and wound cleansing and disinfection.
Finally, the team analyzed the pathogenicity of C. auris by conducting killing assays in G. mellonella. They used a Kaplan-Meier plot to monitor “percent survival” over the course of five days for C. auris, C. glabrata, and C. albicans. Nonaggregative C. auris strains achieved 100% death rate within 48 hours, compared to an approximated 87% death rate from C. albicans. “These data…suggest that the nonaggregative C. auris phenotype has the capacity to form biofilms with enhanced virulence capacity,” Dr Sherry noted. She added that the although it may be possible and, indeed, necessary to implement infection prevention measures targeting C. auris biofilms in patients, on medical devices, and in the hospital environment, additional controls must be researched and implemented in order to prevent the spread of this infection.
Feature Picture Source: Shawn Lockhart / CDC / NCEZID; DFWED; MDB