Disease relevance of Trichosporon

• The absolute stereochemical courses of cis,cis-muconate lactonizing enzyme (MLE;EC 5.5.1.1) from Trichosporon cutaneum (TcMLE) and chloromuconate cycloisomerase (MLE II; EC 5.5.1.7) from Pseudomonas sp B13 have been determined from 1H NMR measurements [1].
• Purification and characterization of the serotype-specific polysaccharide antigen of Trichosporon cutaneum serotype II: a disease-related antigen of Japanese summer-type hypersensitivity pneumonitis [2].
• A novel type of biochemical oxygen demand (BOD) biosensor was developed for water monitor, based on co-immobilizing of Trichosporon cutaneum and Bacillus subtilis in the sol-gel derived composite material which is composed of silica and the grafting copolymer of poly (vinyl alcohol) and 4-vinylpyridine (PVA-g-P(4-VP)) [3].
• Furthermore, C1q (as well as specific IgG and IgA antibody activities to Trichosporon cutaneum antigen) in BALF correlated with clinical symptoms and diffusing capacity (DCO), while the BAL lymphocytosis or the change of OKT4/OKT8 ratio did not [4].
• Fatal Trichosporon pullulans breakthrough fungemia in cancer patients: report of three patients who failed on prophylaxis with itraconazole [5].

High impact information on Trichosporon

• Cryptococcal latex antigen test positive in patient with Trichosporon beigelii infection [6].
• The primary structure of HbpA shares 20.1% sequence identity with phenol 2-monooxygenase from Trichosporon cutaneum [7].
• Properties of anthranilate hydroxylase (deaminating), a flavoprotein from Trichosporon cutaneum [8].
• The other species of Trichosporon did not show high MICs of amphotericin B, and GM MICs were <1 mug/ml [9].
• ER-30346 (MIC90, 0.78 microgram/ml) was four to eight times more active than fluconazole and amphotericin B and had activity comparable to that of itraconazole against Trichosporon beigelli [10].

Chemical compound and disease context of Trichosporon

• Trichosporon beigelii pneumonitis following busulphan-induced leucopenia [11].
• Preparations of the dimeric flavoenzyme phenol hydroxylase derived from Trichosporon cutaneum were found to contain an active tetrameric form when the enzyme was produced in Escherichia coli [12].
• Fungemia due to Trichosporon asahii in a neutropenic child refractory to amphotericin B: clearance with voriconazole [13].
• Fluconazole proved effective in treating fungal peritonitis caused by Trichosporon cutaneum [14].

Biological context of Trichosporon

• The inducible enzyme phenol hydroxylase from Trichosporon cutaneum is a FAD-containing monooxygenase which catalyzes the NADPH-dependent hydroxylation of phenol to catechol [15].
• Detection and quantitation of the glucuronoxylomannan-like polysaccharide antigen from clinical and nonclinical isolates of Trichosporon beigelii and implications for pathogenicity [16].
• Novel ring cleavage products in the biotransformation of biphenyl by the yeast Trichosporon mucoides [17].
• A protopectinase (PPase)-encoding gene, PSE3, from Trichosporon penicillatum was cloned by colony hybridization using two oligonucleotide probes synthesized from the N-terminal amino acid sequences of native PPase SE1 and one peptide from a lysyl endopeptidase digest [18].
• A yeast strain CGMCC 0574, identified as Trichosporon brassicae, was selected from 92 strains for its high (S) selectivity in the hydrolysis of ketoprofen ethyl ester [19].

Anatomical context of Trichosporon

• Demonstration, by immunoelectronmicroscopy, of a cell wall antigen in Trichosporon beigelii that cross-reacts with Cryptococcus neoformans capsular polysaccharide [20].
• Three monoclonal antibodies (MAbs), all of the immunoglobulin G1 subclass, were raised against Cryptococcus neoformans by using the technique of cyclophosphamide ablation of B-cell responses against shared epitopes of the cross-reactive fungus Trichosporon beigelii [21].
• Growth of Candida famata and Trichosporon cutaneum on uric acid as the sole source of carbon and nitrogen was associated with the development of a number of microbodies in the cells [22].
• Effects of macrophage colony-stimulating factor (M-CSF) on anti-fungal activity of mononuclear phagocytes against Trichosporon asahii [23].
• Successful treatment of a Trichosporon beigelii septicemia in a granulocytopenic patient with amphotericin B and granulocyte colony-stimulating factor [24].

Associations of Trichosporon with chemical compounds

• The enzyme catalysing the reduction of maleylacetate to 3-oxoadipate was purified 150-fold from Trichosporon cutaneum, induced for aromatic metabolisms by growth with resorcinol as a major carbon source [25].
• cis,cis-Muconate cyclase from Trichosporon cutaneum [26].
• We assessed the activities of amphotericin B deoxycholate, liposomal amphotericin B, fluconazole, and SCH 39304 against 10 strains of Trichosporon beigelii in mice with hematogenous infections [27].
• Maleylacetate reductase from Trichosporon cutaneum [25].
• Successful treatment of Trichosporon beigelii pneumonia with itraconazole [28].

Gene context of Trichosporon

• Molecular analysis of the Trichosporon cutaneum DSM 70698 argA gene and its use for DNA-mediated transformations [29].
• Molecular phylogenetics of the genus trichosporon inferred from mitochondrial cytochrome B gene sequences [30].
• Eight patients infected with Trichosporon species were treated with fluconazole, SCH 39304, or miconazole for 2-26 weeks [31].
• Sera from patients with systemic infections caused by the opportunistic fungus Trichosporon beigelii have been shown to cross-react with anticryptococcal antibodies [16].
• Trichosporon sp. strain CBS 5581 was identified as Trichosporon pullulans, and one clinical isolate, IFM 48794, was identified as Trichosporon faecale [30].

Analytical, diagnostic and therapeutic context of Trichosporon

• Southern blot analysis revealed the presence of phenol hydroxylase gene-related sequences in a number of T. cutaneum and Trichosporon beigelii strains and in Cryptococcus elinovii but not in Trichosporon pullulans, Trichosporon penicillatum, or Candida tropicalis [32].
• In the experimental infection, amphotericin B, SCH 39304, and fluconazole were effective in prolonging survival and reducing fungal counts in the kidneys of mice infected with a clinical strain of Trichosporon beigelii [31].
• N-Terminal peptide sequence analysis revealed the presence of two nick sites and showed that hydroquinone hydroxylase from C. parapsilosis is structurally related to phenol hydroxylase from Trichosporon cutaneum [33].
• A soluble cytochrome P450 from the yeast Trichosporon cutaneum was purified to homogeneity, using ammonium sulfate fractionation followed by fast protein liquid chromatography (FPLC) with DEAE-cellulose and phenyl-Sepharose columns [34].
• In the microdilution and Etest methods Trichosporon spp. demonstrated relatively high minimum inhibitory concentrations (MICs) for fluconazole (MIC90 4 and 6 microg/ml, respectively) and relatively low MICs for voriconazole (MIC90 0.125 and 0.125 microg/ml, respectively) [35].

References