Rapid detection and identification of Candida albicans and Torulopsis (Candida) glabrata in clinical specimens by species-specific nested PCR amplification of a cytochrome P-450 lanosterol-alpha-demethylase (L1A1) gene fragment

Burgener-Kairuz, Pauline; Zuber, Jean-Philippe; Jaunin, P; Buchman, T. G.; Billé, Jacques; Rossier, Michelle

doi:10.1128/jcm.32.8.1902-1907.1994

Cited by 101 publications

(45 citation statements)

References 20 publications

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“…It should be pointed out, however, that neither of the cited reports presented any data regarding antibody kinetics during the course of infection. Newer techniques such as Candida DNA amplification have produced encouraging results in small studies, and sensitivities of between 60 and 79% for culture-positive clinical specimens have been achieved (3,4,8). Another approach involves a Limulus amoebocyte lysate assay for the detection of elevated levels of 1,3-␤-D-glucan in plasma, which was found to have a sensitivity of 90% for patients with confirmed fungal infection (13).…”

Section: Discussionmentioning

confidence: 99%

Diagnosis of invasive candidiasis in neutropenic children with cancer by determination of D-arabinitol/L-arabinitol ratios in urine

et al. 1997

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Determination of D-arabinitol/L-arabinitol ratios (referred to as D/L-arabinitol ratios) in urine as a tool for the diagnosis of invasive candidiasis was investigated in a prospective study comprising 100 children with cancer. The analyses were made by gas chromatography. Positive D/L-arabinitol ratios were found for 10 of 10 children with confirmed invasive candidiasis, 12 of 23 patients undergoing empiric antifungal chemotherapy, and 4 of 67 children not receiving antifungal treatment. D/L-Arabinitol ratios were positive 3 to 31 days (median, 12 days) before the first culture-positive blood sample was drawn or empiric therapy was initiated. The regular monitoring of D/L-arabinitol ratios in urine holds great promise as a sensitive method for diagnosing invasive candidiasis in immunocompromised children with cancer. Moreover, it may be possible to use an early rise in D/L-arabinitol ratios as a basis for the institution of antifungal chemotherapy and as a means of avoiding unnecessary treatment with potentially toxic antifungal agents.

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Section: Discussionmentioning

confidence: 99%

Diagnosis of invasive candidiasis in neutropenic children with cancer by determination of D-arabinitol/L-arabinitol ratios in urine

et al. 1997

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“…Interspecies variability with respect to 14-␣demethylase binding affinity for azole antifungal agents has been observed. 63,64 Findings such as this may provide insight into at least one of the reasons why some Candida sp are intrinsically less susceptible to specific compounds.…”

Section: Smentioning

confidence: 92%

Antifungal Resistance Among Candida Species

Klepser¹

2001

Pharmacotherapy

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“…All of the genes listed have been cloned in S. cerevisiae (10,83,103). To date, ERG1, ERG2, ERG3, ERG4, ERG7, and ERG11 have been cloned from C. albicans (82,89,92,96,122,174), ERG3 and ERG11 have been cloned from C. glabrata (22,52), and ERG11 has been cloned from C. krusei (22) and C. tropicalis (26). In addition, PRD1, the NADPH-cytochrome P-450 reductase that is important for the function of ERG11, has been cloned from C. albicans (174).…”

Section: Alterations In Other Erg Genesmentioning

confidence: 99%

Clinical, Cellular, and Molecular Factors That Contribute to Antifungal Drug Resistance

1998

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SUMMARY In the past decade, the frequency of diagnosed fungal infections has risen sharply due to several factors, including the increase in the number of immunosuppressed patients resulting from the AIDS epidemic and treatments during and after organ and bone marrow transplants. Linked with the increase in fungal infections is a recent increase in the frequency with which these infections are recalcitrant to standard antifungal therapy. This review summarizes the factors that contribute to antifungal drug resistance on three levels: (i) clinical factors that result in the inability to successfully treat refractory disease; (ii) cellular factors associated with a resistant fungal strain; and (iii) molecular factors that are ultimately responsible for the resistance phenotype in the cell. Many of the clinical factors that contribute to resistance are associated with the immune status of the patient, with the pharmacology of the drugs, or with the degree or type of fungal infection present. At a cellular level, antifungal drug resistance can be the result of replacement of a susceptible strain with a more resistant strain or species or the alteration of an endogenous strain (by mutation or gene expression) to a resistant phenotype. The molecular mechanisms of resistance that have been identified to date in Candida albicans include overexpression of two types of efflux pumps, overexpression or mutation of the target enzyme, and alteration of other enzymes in the same biosynthetic pathway as the target enzyme. Since the study of antifungal drug resistance is relatively new, other factors that may also contribute to resistance are discussed.

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Rapid detection and identification of Candida albicans and Torulopsis (Candida) glabrata in clinical specimens by species-specific nested PCR amplification of a cytochrome P-450 lanosterol-alpha-demethylase (L1A1) gene fragment

Cited by 101 publications

References 20 publications

Diagnosis of invasive candidiasis in neutropenic children with cancer by determination of D-arabinitol/L-arabinitol ratios in urine

Diagnosis of invasive candidiasis in neutropenic children with cancer by determination of D-arabinitol/L-arabinitol ratios in urine

Antifungal Resistance Among Candida Species

Clinical, Cellular, and Molecular Factors That Contribute to Antifungal Drug Resistance

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