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      Simultaneous Emergence of Multidrug-ResistantCandida aurison 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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            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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              Candida haemulonii and closely related species at 5 university hospitals in Korea: identification, antifungal susceptibility, and clinical features.

              Background. Candida haemulonii, a yeast species that often exhibits antifungal resistance, rarely causes human infection. During 2004-2006, unusual yeast isolates with phenotypic similarity to C. haemulonii were recovered from 23 patients (8 patients with fungemia and 15 patients with chronic otitis media) in 5 hospitals in Korea. Methods. Isolates were characterized using D1/D2 domain and ITS gene sequencing, and the susceptibility of the isolates to 6 antifungal agents was tested in vitro. Results. Gene sequencing of the blood isolates confirmed C. haemulonii group I (in 1 patient) and Candida pseudohaemulonii (in 7 patients), whereas all isolates recovered from the ear were a novel species of which C. haemulonii is its closest relative. The minimum inhibitory concentration (MIC) ranges of amphotericin B, fluconazole, itraconazole, and voriconazole for all isolates were 0.5-32 microg/mL (MIC(50), 1 microg/mL), 2-128 microg/mL (MIC(50), 4 microg/mL), 0.125-4 microg/mL (MIC(50), 0.25 microg/mL), and 0.03-2 microg/mL (MIC(50), 0.06 microg/mL), respectively. All isolates were susceptible to caspofungin (MIC, 0.125-0.25 microg/mL) and micafungin (MIC, 0.03-0.06 microg/mL). All cases of fungemia occurred in patients with severe underlying diseases who had central venous catheters. Three patients developed breakthrough fungemia while receiving antifungal therapy, and amphotericin B therapeutic failure, which was associated with a high MIC of amphotericin B (32 microg/mL), was observed in 2 patients. Conclusions. Candida species that are closely related to C. haemulonii are emerging sources of infection in Korea. These species show variable patterns of susceptibility to amphotericin B and azole antifungal agents.
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                Author and article information

                Journal
                Clinical Infectious Diseases
                CLINID
                Oxford University Press (OUP)
                1058-4838
                1537-6591
                January 04 2017
                January 15 2017
                January 15 2017
                October 20 2016
                : 64
                : 2
                : 134-140
                Article
                10.1093/cid/ciw691
                5215215
                27988485
                c4b48f2b-0a47-46fb-94ed-a0e740360de9
                © 2016
                History

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