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      Simultaneous Emergence of Multidrug-Resistant Candida auris on 3 Continents Confirmed by Whole-Genome Sequencing and Epidemiological Analyses.

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          Abstract

          Candida auris, a multidrug-resistant yeast that causes invasive infections, was first described in 2009 in Japan and has since been reported from several countries.

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          First report of Candida auris in America: Clinical and microbiological aspects of 18 episodes of candidemia.

          Characterization of a hospital outbreak of Candida auris candidemia that involved 18 critically ill patients in Venezuela.
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            Prevalence of molecular mechanisms of resistance to azole antifungal agents in Candida albicans strains displaying high-level fluconazole resistance isolated from human immunodeficiency virus-infected patients.

            Molecular mechanisms of azole resistance in Candida albicans, including alterations in the target enzyme and increased efflux of drug, have been described, but the epidemiology of the resistance mechanisms has not been established. We have investigated the molecular mechanisms of resistance to azoles in C. albicans strains displaying high-level fluconazole resistance (MICs, > or =64 microg/ml) isolated from human immunodeficiency virus (HIV)-infected patients with oropharyngeal candidiasis. The levels of expression of genes encoding lanosterol 14alpha-demethylase (ERG11) and efflux transporters (MDR1 and CDR) implicated in azole resistance were monitored in matched sets of susceptible and resistant isolates. In addition, ERG11 genes were amplified by PCR, and their nucleotide sequences were determined in order to detect point mutations with a possible effect in the affinity for azoles. The analysis confirmed the multifactorial nature of azole resistance and the prevalence of these mechanisms of resistance in C. albicans clinical isolates exhibiting frank fluconazole resistance, with a predominance of overexpression of genes encoding efflux pumps, detected in 85% of all resistant isolates, being found. Alterations in the target enzyme, including functional amino acid substitutions and overexpression of the gene that encodes the enzyme, were detected in 65 and 35% of the isolates, respectively. Overall, multiple mechanisms of resistance were combined in 75% of the isolates displaying high-level fluconazole resistance. These results may help in the development of new strategies to overcome the problem of resistance as well as new treatments for this condition.
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              Candida auris–Associated Candidemia, South Africa

              To the Editor: We noted the report by Chowdhary et al. ( 1 ) and report Candida auris as a causative agent of candidemia in South Africa, with an estimated prevalence of 0.3% (N.P. Govender et al., unpub. data). First isolated in 2009, C. auris is an emerging species associated with clinical disease ( 2 – 6 ). We analyzed 4 isolates submitted to the National Institute for Communicable Diseases (Johannesburg, South Africa) from 4 patients with candidemia who had been admitted to different public- and private-sector hospitals from October 2012 through October 2013. Identification of the isolates was undertaken by using ChromAgar Candida medium (Mast Diagnostics, Merseyside, UK), Vitek-2 YST (bioMérieux, Marcy ľEtoile, France), API 20C AUX (bioMérieux), and sequencing of internal transcribed spacer (ITS) and D1/D2 domains of the ribosomal RNA gene ( 7 ), followed by microbroth dilution susceptibility testing ( 8 ). All isolates were misidentified as C. haemulonii and Rhodotorula glutinis by Vitek-2 YST and API 20C AUX assays, respectively (Table). Table Identification and antifungal susceptibility results of 4 Candida auris isolates from 4 male patients with candidemia, South Africa, October 2012–October 2013* Isolate ID Patient age, y Hospital unit Vitek-2 YST† API 20C AUX† DNA sequence analysis‡ MIC AMB FLX VRC POS ITC 5FC CAS MFG AFG 208 85 High-care C. haemulonii Rhodotorula glutinis C. auris 1 >256 0.5 0.03 0.12 0.12 0.25 0.06 0.25 209 60 Medical ICU C. haemulonii R. glutinis C. auris 0.5 >256 1 0.06 0.12 0.12 0.12 0.06 0.12 224 73 Burn C. haemulonii R. glutinis C. auris 1 >256 2 0.06 0.25 0.12 0.25 0.12 0.25 293 27 Trauma ICU C. haemulonii R. glutinis C. auris 1 64 0.25 0.015 0.06 0.06 0.03 0.06 0.06 *AMB, amphotericin B; FLX, fluconazole; VRC, voriconazole; POS, posaconazole; ITC, itraconazole; 5FC, flucytosine; CAS, caspofungin; MFG, micafungin; AFG, anidulafungin.
†bioMérieux, Marcy ľEtoile, France.
‡Sequence data for the 4 isolates have been deposited in GenBank, accession nos. KJ1236762–KJ126765 and KJ126758–KJ126761 for the internal transcribed spacer and D1/D2 regions, respectively. Similar to the findings of Chowdhary et al., all isolates assimilated N-acetyl-glucosamine ( 1 ). With the use of the CBS-KNAW database, pairwise sequence alignment of ITS region showed 99% sequence homology to Kuwait isolates, and alignment of D1/D2 domain showed 98% homology to the Kuwait/India isolates ( 9 ). In a neighbor-joining phylogenetic tree based on ITS sequences, South Africa isolates formed a cluster with India and Kuwait isolates (Technical Appendix Figure). Fluconazole MICs were high for all isolates (Table). Isolates 209 and 224 showed reduced voriconazole susceptibility with MICs of 1 μg/mL and 2 μg/mL, respectively, which is above the epidemiologic cutoff value for 11 Candida species ( 10 ). Isolates were susceptible to amphotericin B and echinocandins at low MICs Clinical data were available for 1 patient (Technical Appendix Table). Two C. haemulonii isolates were identified during laboratory-based sentinel surveillance for candidemia in South Africa; the ITS region of one isolate was sequenced and the isolate identified as C. auris (N.P. Govender, pers. comm.). In this study, C. auris was misidentified by routinely used tests and was accurately identified by sequencing, in keeping with previous findings ( 1 , 3 , 4 , 6 ). Technical Appendix Phylogenetic relatedness of internal transcribed spacer region of the ribosomal RNA gene of Candida auris with closely related Candida species and clinical characteristics of a patient with candidemia caused by C. auris, South Africa.
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                Author and article information

                Journal
                Clin. Infect. Dis.
                Clinical infectious diseases : an official publication of the Infectious Diseases Society of America
                Oxford University Press (OUP)
                1537-6591
                1058-4838
                Jan 15 2017
                : 64
                : 2
                Affiliations
                [1 ] Mycotic Diseases Branch, Centers for Disease Control and Prevention, Atlanta, Georgia; gyi2@cdc.gov.
                [2 ] Mycotic Diseases Branch, Centers for Disease Control and Prevention, Atlanta, Georgia.
                [3 ] Department of Pathology and Laboratory Medicine, Aga Khan University, Karachi, and.
                [4 ] Department of Medical Mycology, Vallabhbhai Patel Chest Institute, University of Delhi, India.
                [5 ] National Institute for Communicable Diseases-Centre for Opportunistic, Tropical and Hospital Infections, a Division of the National Health Laboratory Service, Johannesburg, South Africa.
                [6 ] Division of Infectious Diseases, Federal University of São Paulo-UNIFESP, Brazil.
                [7 ] Department of Infectious Diseases, School of Medicine, Universidad del Zulia, Maracaibo, Venezuela.
                [8 ] Broad Institute, MIT and Harvard, Cambridge, Massachusetts.
                [9 ] JMI Laboratories, North Liberty, Iowa.
                [10 ] Centers for Disease Control and Prevention Field Epidemiology and Laboratory Training Program, Islamabad, Pakistan.
                [11 ] Department of Medical Microbiology and Infectious Diseases, Canisius-Wilhelmina Hospital, and.
                [12 ] Department of Medical Microbiology, Radboudumc, Nijmegen, The Netherlands.
                Article
                ciw691
                10.1093/cid/ciw691
                5215215
                27988485

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