Global epidemiology of emerging Candida auris
Introduction
Since its discovery in 2009 [1•], Candida auris has been identified in more than 30 countries on six continents [2•]. A retrospective SENTRY review identified a 2008 isolation from Pakistan; however, C. auris is generally considered rare before 2009 suggesting that it represents a newly emerging human infection. In contrast to other Candida species, C. auris spreads easily in health-care setting causing nosocomial outbreaks [3,4]. This fungus’ ability to persist, both on the human host and also on inanimate surfaces, has been well documented [5,6] and is likely a key trait explaining its emergence. Exhibiting intrinsic resistance to fluconazole [7•] and variable susceptibility to other azole antifungal drugs, 5-flucytosine [8•], amphotericin B [9], and echinocandins [8•,10,11], C. auris has been widely acknowledged as multi-drug resistant (MDR) [12,13]. This, along with its ability to persist and easily transmit, alongside its highly proliferative clonal life-history, has led to C. auris’ pandemic potential by causing an expanding range of nosocomial infections worldwide [1•,3,7•,14, 15, 16, 17, 18].
Section snippets
Emergence of C. auris
C. auris was first discovered and described in 2009 following isolation from discharge from the ear canal of a patient in Japan [1•] and was taxonomically placed as a close relative to the Candida haemulonii complex. Since its discovery, C. auris has caused a ‘stealthy pandemic’, emerging across the globe (Figure 1) and is now recorded in all continents except Antarctica (Figure 2). However, C. auris is thought to have been misidentified as C. haemulonii on a number of occasions [4,13,19],
Genomic epidemiology
Investigation into the C. auris genome has shown it to possess over 5000 protein coding genes [7•,8•,21], and expresses several virulence factors such as biofilm formation and adherence [22,23], although to a lesser extent than C. albicans [22,24]. Muñoz et al. performed RNA-seq and discovered expansions of entire gene families were linked to drug resistance and virulence [21], which have also been described in C. albicans [25]. Whilst the roles of specific genes were not characterised as part
Antifungal resistance and transmission in C. auris
Currently, candidaemia infections caused by C. albicans are widely managed via the use of echinocandin therapy, and in some cases in combination with amphotericin B [17,32]. Intravenous amphotericin B not in combination with another drug has resulted in treatment failure [15]; however, the mechanistic nature of this resistance is not yet understood. Whilst there are currently no established breakpoints for antifungal susceptibility in C. auris, it is generally accepted that most isolates are
Future directions
Currently, nothing is known about the origins and initial emergence of C. auris; its propensity to survive on inanimate objects within the hospital alongside resistance to disinfection protocols suggests the existence of an unknown non-human environmental reservoir. However, similar to other Candida species, the true nature of C. auris’ ancestral reservoirs currently remains elusive [42, 43, 44]. The detection of clonal C. auris isolates on multiple continents simultaneously with distinct
Acknowledgements
JR and MCF were supported by UK NERC (NE/P001165/1) and the UK MRC (MR/R015600/1). MCF is a Canadian CIFAR Fellow in the ‘Fungal Kingdom’ program.
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