Disease relevance of Candida

• We tested 170 patients at high risk for invasive candidiasis for candida enolase antigenemia [1].
• More recently, fluconazole, a water-soluble triazole with activity against candida species and little toxicity, has become available [2].
• In addition, fluconazole is effective for selected patients with serious candida syndromes such as candidemia, and itraconazole is the most effective of the azoles for the treatment of aspergillosis [3].
• The positive skin tests to PPD, candida and mumps persisted [4].
• Fluconazole versus itraconazole for candida esophagitis in acquired immunodeficiency syndrome. Candida Esophagitis [5].

High impact information on Candida

• This Candida cph1/cph1 efg1/efg1 double mutant, locked in the yeast form, is avirulent in a mouse model [6].
• Subjects with anergy (0 mm induration in reaction to PPD and candida antigens) were randomly assigned to receive either placebo (323 subjects) or six months of isoniazid (395) [7].
• Initial findings suggested that the presence of candida enolase in the blood may be a novel marker for invasive candidiasis [1].
• Candida enolase antigenemia is a novel marker for invasive candidiasis [1].
• Candida albicans mutants lacking ICL1 are markedly less virulent in mice than the wild type [8].

Chemical compound and disease context of Candida

• Ketoconazole-resistant Candida esophagitis in patients with acquired immunodeficiency syndrome [9].
• To demonstrate the applicability of this method, in vivo modification was performed on 5S rRNA in both Escherichia coli and Candida albicans with 1-cyclohexyl-3-(2-morpholinoethyl) carbodiimide metho-p-toluene sulfonate, dimethyl sulfate, and kethoxal [10].
• Four of the six mitral xenografts associated with thromboembolism were in the 16 patients who had atrial fibrillation and received aspirin and dipyridamole but no warfarin (12% per patient-year), and two were in the 14 patients who were in sinus rhythm and were not taking medication, one of whom had recurrent Candida endocarditis [11].
• Taxol (10(-5) M) decreased killing of Staphylococcus aureus, but did not alter phagocytosis of heat-killed Candida or hexose monophosphate shunt activity in resting or stimulated PMN [12].
• Handicaps to host defense. Effects of hyperglycemia on C3 and Candida albicans [13].

Biological context of Candida

• Molecular mimicry in Candida albicans. Role of an integrin analogue in adhesion of the yeast to human endothelium [14].
• Cells of the reactive clone did not mediate increased monocyte PCA in response to Candida, even though peripheral blood mononuclear cells from the donor demonstrated increased PCA to both Candida and PPD [15].
• Hgc1, a novel hypha-specific G1 cyclin-related protein regulates Candida albicans hyphal morphogenesis [16].
• NRG1 represses yeast-hypha morphogenesis and hypha-specific gene expression in Candida albicans [17].
• We have analyzed the role of chitin, a cell-wall polysaccharide, in the virulence of Candida albicans [18].

Anatomical context of Candida

• Activation of macrophages for enhanced release of superoxide anion and greater killing of Candida albicans by injection of muramyl dipeptide [19].
• The antigen used was purified from the cell wall of Candida albicans strain A and contained greater than 96% polysaccharide mannan [20].
• We have now generated MPO-deficient mice, and show here that neutrophils from homozygous mutants lack peroxidase and chlorination activity in vitro and fail to generate chlorotyrosine or to kill Candida albicans in vivo [21].
• Human T lymphocytes sensitized to Candida albicans (CA) were shown to proliferate in cultures induced with mannan, a ramified polysaccharide extracted from the cell well of CA [22].
• We tested the in vitro susceptibility of Candida albicans to three defensins from human neutrophilic granulocytes (HNP-1, 2, and 3), a homologous defensin from rabbit leukocytes (NP-1), and four unrelated cationic peptides [23].

Associations of Candida with chemical compounds

• The bloodstream infection failed to clear in 12 patients in the amphotericin group and 15 in the fluconazole group; the species most commonly associated with failure was Candida albicans [2].
• The codon CUG is read as serine in an asporogenic yeast Candida cylindracea [24].
• Here we report another example of divergence from the universal code, this time in a non-spore-forming yeast Candida cylindracea, in which the universal codon for leucine, CUG, is used to code for serine [24].
• D-Arabinitol was identified as a major metabolite of Candida species in human subjects [25].
• Flucytosine treatment of Candida arthritis [26].

Gene context of Candida

• Control of filament formation in Candida albicans by the transcriptional repressor TUP1 [27].
• Suppression of hyphal formation in Candida albicans by mutation of a STE12 homolog [28].
• Virulence-related surface glycoproteins in the yeast pathogen Candida glabrata are encoded in subtelomeric clusters and subject to RAP1- and SIR-dependent transcriptional silencing [29].
• Phenotypic switching in Candida albicans is controlled by a SIR2 gene [30].
• In the dimorphic fungus Candida albicans, the CHS2 gene encodes a chitin synthase that is expressed preferentially in the hyphal form [31].

Analytical, diagnostic and therapeutic context of Candida

• We detected antigen using a double-sandwich liposomal immunoassay for candida enolase in serially collected serum samples [1].
• Molecular cloning and characterization of chitinase genes from Candida albicans [32].
• Affinity chromatography and further characterization of the glucosyltransferases involved in hydroxydocosanoic acid sophoroside production in Candida bogoriensis [33].
• Peroxisomes have been purified from Candida tropicalis grown on oleic acid and shown to be nearly pure by marker enzyme analysis, electron microscopy, and comparative sodium dodecyl sulfate-polyacrylamide gel electrophoresis [34].
• DNA array studies demonstrate convergent regulation of virulence factors by Cph1, Cph2, and Efg1 in Candida albicans [35].

References