{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:16:08Z","timestamp":1787015768658,"version":"build-2736575974"},"reference-count":49,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2021,5,15]],"date-time":"2021-05-15T00:00:00Z","timestamp":1621036800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Mycoses"],"published-print":{"date-parts":[[2021,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      <jats:italic>Candida parapsilosis<\/jats:italic>\n                      complex consists of three species, the prevalence and geographical distribution of which might vary. Increasing rates of fluconazole resistance among\n                      <jats:italic>C.\u00a0parapsilosis<\/jats:italic>\n                      complex were reported from various centres.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>\n                      Aim of this study was to identify invasive\n                      <jats:italic>C.\u00a0parapsilosis<\/jats:italic>\n                      complex strains up to species level, explore rates and molecular mechanisms of azole resistance and analyse temporal changes at a single centre.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Isolates from blood cultures from 1997 to 2017 were included. Species were identified using RFLP of the\n                      <jats:italic>SADH<\/jats:italic>\n                      gene and confirmed with\n                      <jats:italic>ITS<\/jats:italic>\n                      sequencing when needed. In vitro susceptibility to fluconazole, voriconazole and posaconazole was tested and evaluated using EUCAST guidelines. Sequences of\n                      <jats:italic>ERG11<\/jats:italic>\n                      and\n                      <jats:italic>MRR1<\/jats:italic>\n                      genes were analysed for fluconazole non\u2010susceptible isolates.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      A total of 283 isolates from 181 patients were tested for azole susceptibility. All were\n                      <jats:italic>C.\u00a0parapsilosis<\/jats:italic>\n                      sensu\n                      <jats:italic>stricto<\/jats:italic>\n                      , except one\n                      <jats:italic>C.\u00a0orthopsilosis<\/jats:italic>\n                      . All three azoles were effective against 213 of the isolates from 135 patients, including one\n                      <jats:italic>C.\u00a0orthopsilosis<\/jats:italic>\n                      . Fluconazole resistance was 13.3% (24\/181 patients). While the first fluconazole\u2010resistant isolates were detected in 2004, increase was evident after 2011. In\n                      <jats:italic>ERG11<\/jats:italic>\n                      , Y132F mutation was the most common among fluconazole non\u2010susceptible isolates (71.7%), followed by G458S (10.9%) and D421N (4.3%). In MRR1, R405K (56.5%) and G927C (8.7%) were detected. However, association of these mutations to azole resistance is yet to be investigated.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Rising azole resistance rates in\n                      <jats:italic>C.\u00a0parapsilosis<\/jats:italic>\n                      sensu\n                      <jats:italic>stricto<\/jats:italic>\n                      isolates particularly after 2011 were of concern. The well\u2010known Y132F mutation was the predominant mechanism of azole resistance while accompanied with other genetic mutations.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/myc.13296","type":"journal-article","created":{"date-parts":[[2021,5,2]],"date-time":"2021-05-02T03:35:17Z","timestamp":1619926517000},"page":"823-830","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":35,"title":["Species distribution, azole resistance and related molecular mechanisms in invasive\n                    <i>Candida parapsilosis<\/i>\n                    complex isolates: Increase in fluconazole resistance in 21 years"],"prefix":"10.1111","volume":"64","author":[{"given":"Selay","family":"Demirci\u2010Duarte","sequence":"first","affiliation":[{"name":"Medical Microbiology Department Hacettepe University Faculty of Medicine Ankara Turkey"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sevtap","family":"Arikan\u2010Akdagli","sequence":"additional","affiliation":[{"name":"Medical Microbiology Department Hacettepe University Faculty of Medicine Ankara Turkey"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9021-0439","authenticated-orcid":false,"given":"Dolunay","family":"G\u00fclmez","sequence":"additional","affiliation":[{"name":"Medical Microbiology Department Hacettepe University Faculty of Medicine Ankara Turkey"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2021,5,15]]},"reference":[{"issue":"1","key":"e_1_2_9_2_1","first-page":"S79","article-title":"Twenty years of the SENTRY antifungal surveillance program: results for Candida species from 1997\u20132016. 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