Risk assessment of arterial allograft contamination from tissue donors colonized by Candida auris

Photodynamic Inactivation Effectively Eradicates Candida auris Biofilm despite Its Interference with the Upregulation of CDR1 and MDR1 Efflux Genes

“…C. auris was already described to cause illness in patients more than a decade ago; nevertheless, its surge in incidence at the global level is alarming [1,2]. The majority of clinical isolates of C. auris manifest resistance to one or more main classes of antifungals-azoles, echinocandins, and polyenes [3][4][5]. Further complications are promoted by C. auris thermotolerance, osmotolerance, and resistance to disinfectants [6].…”

Candida auris: A Quick Review on Identification, Current Treatments, and Challenges

“…The majority of clinical C. auris isolates display resistance to main classes of antifungals (azoles, polyenes, or echinocandins), and there is multi (MDR)- or pan-drug resistance to more than two antifungal classes [ 13 ]. Many research groups have studied the molecular mechanisms implicated in resistance development, resulting in limited therapeutic options [ 13 , 78 ]. As previously noted, in order to not fail in treatment of C. auris infections, accurate detection and identification of this pathogen is necessary [ 35 , 78 ].…”

“…Generally, whole-genome sequencing of resistant isolates has identified four novel nonsynonymous mutations, emphasizing a probable correlation with AmB resistance. The reduction in ergosterol content in the cellular membrane [ 13 , 25 ] is due to overexpression of several mutated ERG genes [ 81 ]. These mutations included those in genes with homology to the transcription factor FLO8 gene of C. albicans and a membrane transporter [ 94 ].…”

“…The development of resistance to echinocandins is rare, and they are the first-line therapy drugs against C. auris infections [ 13 , 25 ]. This resistance is typically associated with hot spot mutations in the FKS1 gene, which encodes the (1,3)-β-D-glucan synthase enzyme, the target of echinocandins, resulting in lower affinity of the enzyme to the drug [ 76 ].…”

“…The most worrisome aspects associated with infection caused by C. auris can be summarized in three levels: High rate of antifungal drug resistance [ 9 ], mode and pace of its easy transmission among healthcare workers and patients in hospitals, and misidentification. This last level is related to difficulties in a correct identification of C. auris strains, which are commonly misidentified as other phylogenetically-related pathogens, but also due to inadequacies of common diagnostic tools to precise identification of C. auris in many countries that result in misidentification and incorrect therapy, which lead to the acquisition of multiple genetic determinants that confer multidrug resistance [ 11 , 12 , 13 , 14 ].…”