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  1. Article ; Online: Candida albicans

    Yadav, Anshuman / Sah, Sudisht K / Perlin, David S / Rustchenko, Elena

    Journal of fungi (Basel, Switzerland)

    2024  Volume 10, Issue 3

    Abstract: The opportunistic ... ...

    Abstract The opportunistic fungus
    Language English
    Publishing date 2024-03-19
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2784229-0
    ISSN 2309-608X ; 2309-608X
    ISSN (online) 2309-608X
    ISSN 2309-608X
    DOI 10.3390/jof10030224
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Deciphering Candida auris Paradoxical Growth Effect (Eagle Effect) in Response to Echinocandins.

    Kordalewska, Milena / Perlin, David S

    Methods in molecular biology (Clifton, N.J.)

    2022  Volume 2517, Page(s) 73–85

    Abstract: The paradoxical growth effect (PGE; also known as Eagle effect) is an in vitro phenomenon observed during antifungal susceptibility testing (AFST). In PGE, some fungal isolates grow in medium containing high concentrations of an echinocandin, above the ... ...

    Abstract The paradoxical growth effect (PGE; also known as Eagle effect) is an in vitro phenomenon observed during antifungal susceptibility testing (AFST). In PGE, some fungal isolates grow in medium containing high concentrations of an echinocandin, above the minimal inhibitory concentration (MIC), despite being fully susceptible at lower concentrations. The presence of PGE complicates the assignment of isolates to susceptible or resistant category, especially in the case of newly emerged pathogens like Candida auris, for which susceptibility breakpoints are not established.Here we describe a protocol aiding in the determination of whether a given C. auris isolate is echinocandin-resistant or echinocandin-susceptible but exhibiting paradoxical growth.
    MeSH term(s) Antifungal Agents/pharmacology ; Candida auris/drug effects ; Drug Resistance, Fungal ; Echinocandins/pharmacology ; Microbial Sensitivity Tests
    Chemical Substances Antifungal Agents ; Echinocandins
    Language English
    Publishing date 2022-06-08
    Publishing country United States
    Document type Journal Article
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-0716-2417-3_6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Detection and Identification of Candida auris from Clinical Skin Swabs.

    Kordalewska, Milena / Perlin, David S

    Methods in molecular biology (Clifton, N.J.)

    2022  Volume 2542, Page(s) 245–256

    Abstract: Candida auris is a recently emerged pathogenic fungus posing an urgent global health threat. Given its propensity to cause nosocomial outbreaks, rapid detection and accurate identification of C. auris have become essential for an effective implementation ...

    Abstract Candida auris is a recently emerged pathogenic fungus posing an urgent global health threat. Given its propensity to cause nosocomial outbreaks, rapid detection and accurate identification of C. auris have become essential for an effective implementation of infection prevention and control measures in healthcare facilities. Unfortunately, the requirement of culturing a yeast colony from a patient sample, central for most of the available diagnostic tools, results in substantial delays (several days or longer) in diagnosis. However, nucleic acid-based techniques can deliver accurate diagnostic results within several hours since they are based on analysis of DNA extracted from patient specimen (no need of culture).Here we describe a real-time PCR assay protocol which can be applied for C. auris detection and identification directly from patient swabs.
    MeSH term(s) Antifungal Agents ; Candida/genetics ; Candida auris ; Candidiasis/diagnosis ; Candidiasis/microbiology ; Humans ; Real-Time Polymerase Chain Reaction/methods
    Chemical Substances Antifungal Agents
    Language English
    Publishing date 2022-08-25
    Publishing country United States
    Document type Journal Article
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-0716-2549-1_18
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  4. Article: Cell Wall-Modifying Antifungal Drugs.

    Perlin, David S

    Current topics in microbiology and immunology

    2019  Volume 425, Page(s) 255–275

    Abstract: Antifungal therapy is a critical component of patient management for invasive fungal diseases. Yet, therapeutic choices are limited as only a few drug classes are available to treat systemic disease, and some infecting strains are resistant to one or ... ...

    Abstract Antifungal therapy is a critical component of patient management for invasive fungal diseases. Yet, therapeutic choices are limited as only a few drug classes are available to treat systemic disease, and some infecting strains are resistant to one or more drug classes. The ideal antifungal inhibits a fungal-specific essential target not present in human cells to avoid off-target toxicities. The fungal cell wall is an ideal drug target because its integrity is critical to cell survival and a majority of biosynthetic enzymes and wall components is unique to fungi. Among currently approved antifungal agents and those in clinical development, drugs targeting biosynthetic enzymes of the cell wall show safe and efficacious antifungal properties, which validates the cell wall as a target. The echinocandins, which inhibit β-1,3-glucan synthase, are recommended as first-line therapy for Candida infections. Newer cell wall-active drugs in clinical development encompass next-generation glucan synthase inhibitors including a novel echinocandin and an enfumafungin, an inhibitor of Gwt1, a key component of GPI anchor protein biosynthesis, and a classic inhibitor of chitin biosynthesis. As the cell wall is rich in potential drug discovery targets, it is primed to help deliver the next generation of antifungal drugs.
    MeSH term(s) Antifungal Agents/pharmacology ; Antifungal Agents/therapeutic use ; Candidiasis/drug therapy ; Candidiasis/microbiology ; Cell Wall/drug effects ; Echinocandins/pharmacology ; Echinocandins/therapeutic use ; Fungi/cytology ; Fungi/drug effects ; Humans
    Chemical Substances Antifungal Agents ; Echinocandins
    Language English
    Publishing date 2019-12-14
    Publishing country Germany
    Document type Journal Article ; Review
    ZDB-ID 210099-X
    ISSN 0070-217X
    ISSN 0070-217X
    DOI 10.1007/82_2019_188
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    In stock of ZB MED Cologne/Königswinter

    Ud II Zs.24: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  5. Article ; Online: Reactive oxidant species induced by antifungal drugs: identity, origins, functions, and connection to stress-induced cell death.

    Gonzalez-Jimenez, Irene / Perlin, David S / Shor, Erika

    Frontiers in cellular and infection microbiology

    2023  Volume 13, Page(s) 1276406

    Abstract: Reactive oxidant species (ROS) are unstable, highly reactive molecules that are produced by cells either as byproducts of metabolism or synthesized by specialized enzymes. ROS can be detrimental, e.g., by damaging cellular macromolecules, or beneficial, ... ...

    Abstract Reactive oxidant species (ROS) are unstable, highly reactive molecules that are produced by cells either as byproducts of metabolism or synthesized by specialized enzymes. ROS can be detrimental, e.g., by damaging cellular macromolecules, or beneficial, e.g., by participating in signaling. An increasing body of evidence shows that various fungal species, including both yeasts and molds, increase ROS production upon exposure to the antifungal drugs currently used in the clinic: azoles, polyenes, and echinocandins. However, the implications of these findings are still largely unclear due to gaps in knowledge regarding the chemical nature, molecular origins, and functional consequences of these ROS. Because the detection of ROS in fungal cells has largely relied on fluorescent probes that lack specificity, the chemical nature of the ROS is not known, and it may vary depending on the specific fungus-drug combination. In several instances, the origin of antifungal drug-induced ROS has been identified as the mitochondria, but further experiments are necessary to strengthen this conclusion and to investigate other potential cellular ROS sources, such as the ER, peroxisomes, and ROS-producing enzymes. With respect to the function of the ROS, several studies have shown that they contribute to the drugs' fungicidal activities and may be part of drug-induced programmed cell death (PCD). However, whether these "pro-death" ROS are a primary consequence of the antifungal mechanism of action or a secondary consequence of drug-induced PCD remains unclear. Finally, several recent studies have raised the possibility that ROS induction can serve an adaptive role, promoting antifungal drug tolerance and the evolution of drug resistance. Filling these gaps in knowledge will reveal a new aspect of fungal biology and may identify new ways to potentiate antifungal drug activity or prevent the evolution of antifungal drug resistance.
    MeSH term(s) Antifungal Agents/pharmacology ; Antifungal Agents/therapeutic use ; Reactive Oxygen Species/metabolism ; Oxidants ; Echinocandins/pharmacology ; Apoptosis
    Chemical Substances Antifungal Agents ; Reactive Oxygen Species ; Oxidants ; Echinocandins
    Language English
    Publishing date 2023-10-12
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 2619676-1
    ISSN 2235-2988 ; 2235-2988
    ISSN (online) 2235-2988
    ISSN 2235-2988
    DOI 10.3389/fcimb.2023.1276406
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  6. Article ; Online: DNA damage response of major fungal pathogen Candida glabrata offers clues to explain its genetic diversity.

    Shor, Erika / Perlin, David S

    Current genetics

    2021  Volume 67, Issue 3, Page(s) 439–445

    Abstract: ... pathogen and host and the evolution of antifungal drug resistance. A close relative of S. cerevisiae ... damage response of S. cerevisiae. First, we discovered that, in contrast to the established paradigm, C ... accumulate in S-phase and proceeded with cell division, leading to aberrant mitoses and cell death. Finally ...

    Abstract How cells respond to DNA damage is key to maintaining genome integrity or facilitating genetic change. In fungi, DNA damage responses have been extensively characterized in the model budding yeast Saccharomyces cerevisiae, which is generally not pathogenic. However, it is not clear how closely these responses resemble those in fungal pathogens, in which genetic change plays an important role in the evolutionary arms race between pathogen and host and the evolution of antifungal drug resistance. A close relative of S. cerevisiae, Candida glabrata, is an opportunistic pathogen that displays high variability in chromosome structure among clinical isolates and rapidly evolves antifungal drug resistance. The mechanisms facilitating such genomic flexibility and evolvability in this organism are unknown. Recently we characterized the DNA damage response of C. glabrata and identified several features that distinguish it from the well characterized DNA damage response of S. cerevisiae. First, we discovered that, in contrast to the established paradigm, C. glabrata effector kinase Rad53 is not hyperphosphorylated upon DNA damage. We also uncovered evidence of an attenuated DNA damage checkpoint response, wherein in the presence of DNA damage C. glabrata cells did not accumulate in S-phase and proceeded with cell division, leading to aberrant mitoses and cell death. Finally, we identified evidence of transcriptional rewiring of the DNA damage response of C. glabrata relative to S. cerevisiae, including an upregulation of genes involved in mating and meiosis-processes that have not been reported in C. glabrata. Together, these results open new possibilities and raise tantalizing questions of how this major fungal pathogen facilitates genetic change.
    MeSH term(s) Candida glabrata/genetics ; Candida glabrata/pathogenicity ; Candidiasis/genetics ; Candidiasis/microbiology ; DNA Damage/genetics ; Drug Resistance, Fungal/genetics ; Genes, Mating Type, Fungal/genetics ; Genetic Variation/genetics ; Humans ; Meiosis/genetics
    Language English
    Publishing date 2021-02-23
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 282876-5
    ISSN 1432-0983 ; 0172-8083
    ISSN (online) 1432-0983
    ISSN 0172-8083
    DOI 10.1007/s00294-021-01162-7
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2586: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  7. Article ; Online: Review of the Novel Echinocandin Antifungal Rezafungin: Animal Studies and Clinical Data.

    Zhao, Yanan / Perlin, David S

    Journal of fungi (Basel, Switzerland)

    2020  Volume 6, Issue 4

    Abstract: Rezafungin is a novel echinocandin drug being developed as a first-line option for treatment and prevention of invasive fungal infections. As a result of a structural modification in its parent molecule anidulafungin, rezafungin has acquired unique ... ...

    Abstract Rezafungin is a novel echinocandin drug being developed as a first-line option for treatment and prevention of invasive fungal infections. As a result of a structural modification in its parent molecule anidulafungin, rezafungin has acquired unique chemical stability conferring prolonged pharmacokinetics, as well as an administration advantage in the clinical setting compared to other drugs in the same class. Rezafungin displays potent in vitro activity against a wide spectrum of fungal pathogens, which is reflected in robust in vivo efficacy and/or pharmacodynamic studies using various animal models as well as in promising clinical trials data. This review describes in vivo characterization of rezafungin using animal models, current status of clinical development and key findings from these studies.
    Language English
    Publishing date 2020-09-28
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2784229-0
    ISSN 2309-608X ; 2309-608X
    ISSN (online) 2309-608X
    ISSN 2309-608X
    DOI 10.3390/jof6040192
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  8. Article: Identification of Drug Resistant

    Kordalewska, Milena / Perlin, David S

    Frontiers in microbiology

    2019  Volume 10, Page(s) 1918

    Abstract: ... Candida ... ...

    Abstract Candida auris
    Language English
    Publishing date 2019-08-20
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2587354-4
    ISSN 1664-302X
    ISSN 1664-302X
    DOI 10.3389/fmicb.2019.01918
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  9. Article: Echinocandin Resistance in

    Satish, Shruthi / Perlin, David S

    Microbiology insights

    2019  Volume 12, Page(s) 1178636119897034

    Abstract: Echinocandin drugs target the fungal enzyme β-(1,3)-glucan synthase (GS), which is required for the synthesis of cell wall component β-(1,3)-d-glucan. They are first-line therapy ... ...

    Abstract Echinocandin drugs target the fungal enzyme β-(1,3)-glucan synthase (GS), which is required for the synthesis of cell wall component β-(1,3)-d-glucan. They are first-line therapy for
    Language English
    Publishing date 2019-12-31
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2455264-1
    ISSN 1178-6361
    ISSN 1178-6361
    DOI 10.1177/1178636119897034
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  10. Article ; Online: Molecular Diagnostics in the Times of Surveillance for

    Kordalewska, Milena / Perlin, David S

    Journal of fungi (Basel, Switzerland)

    2019  Volume 5, Issue 3

    Abstract: Recently, global health professionals have been significantly challenged by the emergence ... ...

    Abstract Recently, global health professionals have been significantly challenged by the emergence of
    Language English
    Publishing date 2019-08-20
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2784229-0
    ISSN 2309-608X ; 2309-608X
    ISSN (online) 2309-608X
    ISSN 2309-608X
    DOI 10.3390/jof5030077
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