title: Fluconazole-resistant pathogens Candida inconspicua and C. norvegensis: DNA sequence diversity of the rRNA intergenic spacer region, antifungal drug susceptibility, and extracellular enzyme production.
abstract: The opportunistic fungal pathogens Candida inconspicua and C. norvegensis are very rarely isolated from patients and are resistant to fluconazole. We collected 38 strains of the two microorganisms isolated from Europe and Japan, and compared the polymorphism of the rRNA intergenic spacer (IGS) and internal transcribed spacer (ITS) regions, antifungal drug susceptibility, and extracellular enzyme production as a potential virulence factor. While the IGS sequences of C. norvegensis were not very divergent (more than 96.7% sequence similarity among the strains), those of C. inconspicua showed remarkable diversity, and were divided into four genotypes with three subtypes. In the ITS region, no variation was found in either species. Since the sequence similarity of the two species is approximately 70% at the ITS region, they are closely related phylogenetically. Fluconazole resistance was reconfirmed for the two microorganisms but they were susceptible to micafungin and amphotericin B. No strain of either species secreted aspartyl proteinase or phospholipase B. These results provide basal information for accurate identification, which is of benefit to global molecular epidemiological studies and facilitates our understanding of the medical mycological characteristics of C. inconspicua and C. norvegensis.
authors.affiliation: Department of Microbiology, Meiji Pharmaceutical University, Kiyose, Tokyo, Japan. sugita@my-pharm.ac.jp
authors.forename: Takashi
authors.initials: T
authors.lastname: Sugita
authors.forename: Kanji
authors.initials: K
authors.lastname: Takeo
authors.forename: Misako
authors.initials: M
authors.lastname: Ohkusu
authors.forename: Eric
authors.initials: E
authors.lastname: Virtudazo
authors.forename: Masako
authors.initials: M
authors.lastname: Takashima
authors.forename: Emi
authors.initials: E
authors.lastname: Asako
authors.forename: Fumiko
authors.initials: F
authors.lastname: Ohshima
authors.forename: Satoshi
authors.initials: S
authors.lastname: Harada
authors.forename: Chikako
authors.initials: C
authors.lastname: Yanaka
authors.forename: Akemi
authors.initials: A
authors.lastname: Nishikawa
authors.forename: Laszlo
authors.initials: L
authors.lastname: Majoros
authors.forename: Matthias
authors.initials: M
authors.lastname: Sipiczki
mesh_terms: D000666:Amphotericin B / Q000494:pharmacology; D000935:Antifungal Agents / Q000494:pharmacology*; D016282:Aspartic Acid Endopeptidases / Q000378:metabolism*; D001483:Base Sequence; D002175:Candida / Q000145:classification / Q000187:drug effects* / Q000201:enzymology / Q000235:genetics; D021903:DNA, Ribosomal Spacer / Q000032:analysis*; D025141:Drug Resistance, Fungal; D054714:Echinocandins; D015725:Fluconazole / Q000494:pharmacology*; D014644:Genetic Variation; D055666:Lipopeptides; D008074:Lipoproteins / Q000494:pharmacology; D008245:Lysophospholipase / Q000378:metabolism*; D000077551:Micafungin; D008969:Molecular Sequence Data; D010456:Peptides, Cyclic / Q000494:pharmacology; D012335:RNA, Ribosomal / Q000235:genetics; D014774:Virulence / Q000235:genetics
chemical_list: D000935:Antifungal Agents; D021903:DNA, Ribosomal Spacer; D054714:Echinocandins; D055666:Lipopeptides; D008074:Lipoproteins; D010456:Peptides, Cyclic; D012335:RNA, Ribosomal; D000666:Amphotericin B; D015725:Fluconazole; D008245:Lysophospholipase; D016282:Aspartic Acid Endopeptidases; D000077551:Micafungin