title: Susceptibility patterns and molecular identification of Trichosporon species.
abstract: The physiological patterns, the sequence polymorphisms of the internal transcriber spacer (ITS), and intergenic spacer regions (IGS) of the rRNA genes and the antifungal susceptibility profile were evaluated for their ability to identify Trichosporon spp. and their specificity for the identification of 49 clinical isolates of Trichosporon spp. Morphological and biochemical methodologies were unable to differentiate among the Trichosporon species. ITS sequencing was also unable to differentiate several species. However, IGS1 sequencing unambiguously identified all Trichosporon isolates. Following the results of DNA-based identification, Trichosporon asahii was the species most frequently isolated from deep sites (15 of 25 strains; 60%). In the main, other Trichosporon species were recovered from cutaneous samples. The majority of T. asahii, T. faecale, and T. coremiiforme clinical isolates exhibited resistance in vitro to amphotericin B, with geometric mean (GM) MICs >4 mug/ml. The other species of Trichosporon did not show high MICs of amphotericin B, and GM MICs were <1 mug/ml. Azole agents were active in vitro against the majority of clinical strains. The most potent compound in vitro was voriconazole, with a GM MIC </=0.14 mug/ml. The sequencing of IGS correctly identified Trichosporon isolates; however, this technique is not available in many clinical laboratories, and strains should be dispatched to reference centers where these complex methods are available. Therefore, it seems to be more practical to perform antifungal susceptibility testing of all isolates belonging to Trichosporon spp., since correct identification could take several weeks, delaying the indication of an antifungal agent which exhibits activity against the infectious strain.
authors.affiliation: Servicio de Micología, Centro Nacional de Microbiología, Instituto de Salud Carlos III, Majadahonda, Madrid, Spain. juanl.rodriguez-tudela@isciii.es
authors.forename: Juan L
authors.initials: JL
authors.lastname: Rodriguez-Tudela
authors.forename: Teresa M
authors.initials: TM
authors.lastname: Diaz-Guerra
authors.forename: Emilia
authors.initials: E
authors.lastname: Mellado
authors.forename: Virginia
authors.initials: V
authors.lastname: Cano
authors.forename: Cecilia
authors.initials: C
authors.lastname: Tapia
authors.forename: Alexander
authors.initials: A
authors.lastname: Perkins
authors.forename: Alicia
authors.initials: A
authors.lastname: Gomez-Lopez
authors.forename: Laura
authors.initials: L
authors.lastname: Rodero
authors.forename: Manuel
authors.initials: M
authors.lastname: Cuenca-Estrella
mesh_terms: D000666:Amphotericin B / Q000494:pharmacology; D000935:Antifungal Agents / Q000494:pharmacology; D001118:Argentina / Q000453:epidemiology; D004271:DNA, Fungal / Q000032:analysis / Q000235:genetics; D021901:DNA, Intergenic / Q000032:analysis / Q000235:genetics; D004275:DNA, Ribosomal / Q000032:analysis / Q000235:genetics; D021903:DNA, Ribosomal Spacer / Q000032:analysis / Q000235:genetics; D004198:Disease Susceptibility; D025141:Drug Resistance, Fungal / Q000235:genetics; D006801:Humans; D008826:Microbial Sensitivity Tests; D010802:Phylogeny; D011110:Polymorphism, Genetic; D012331:RNA, Fungal / Q000032:analysis / Q000235:genetics; D012335:RNA, Ribosomal / Q000032:analysis / Q000235:genetics; D012189:Retrospective Studies; D017422:Sequence Analysis, DNA; D013030:Spain / Q000453:epidemiology; D014250:Trichosporon / Q000145:classification* / Q000187:drug effects / Q000235:genetics* / Q000254:growth & development / Q000302:isolation & purification / Q000502:physiology*
chemical_list: D000935:Antifungal Agents; D004271:DNA, Fungal; D021901:DNA, Intergenic; D004275:DNA, Ribosomal; D021903:DNA, Ribosomal Spacer; D012331:RNA, Fungal; D012335:RNA, Ribosomal; D000666:Amphotericin B