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Whole Genome Sequencing of Candida glabrata for Detection of Markers of Antifungal Drug Resistance
08:45

Whole Genome Sequencing of Candida glabrata for Detection of Markers of Antifungal Drug Resistance

Published on: December 28, 2017

Drug resistance in the opportunistic pathogens Candida albicans and Candida glabrata

D Kerridge, R O Nicholas

    The Journal of Antimicrobial Chemotherapy
    |October 1, 1986
    PubMed

    Insights

    Antifungal drug resistance in Candida albicans varies by drug class. While resistance to polyenes and imidazoles is rare, 5-fluorocytosine resistance is a significant clinical issue due to genetic mechanisms.

    Area of Science:

    • Mycology
    • Medical Mycology
    • Antimicrobial Resistance

    Background:

    • Candida albicans is a major cause of topical and systemic fungal infections.
    • Antifungal drugs are crucial for treating these infections, with polyenes, imidazoles, and 5-fluorocytosine being key agents.
    • Understanding drug resistance mechanisms is vital for effective treatment strategies.

    Purpose of the Study:

    • To compare the mechanisms and clinical significance of drug resistance in Candida albicans for different antifungal drug classes.
    • To investigate the genetic basis of resistance to 5-fluorocytosine in Candida albicans.

    Main Methods:

    • Analysis of drug interaction with fungal membranes for polyene and imidazole antifungals.
    • Genetic analysis of Candida albicans mutants resistant to 5-fluorocytosine, focusing on UMP pyrophosphorylase.
    • Comparison with resistance mechanisms in other pathogens, such as acyclovir resistance in herpes simplex virus.

    Main Results:

    • Mutants of Candida albicans resistant to polyene macrolides and imidazole derivatives are not a significant clinical problem.
    • Resistance to 5-fluorocytosine is a serious clinical issue in Candida albicans.
    • Partial resistance to 5-fluorocytosine is linked to heterozygosity for UMP pyrophosphorylase, with homozygous resistance arising from enzyme absence.

    Conclusions:

    • The diploid nature and complex drug-target interactions of Candida albicans limit resistance to polyenes and imidazoles.
    • The genetic mechanisms underlying 5-fluorocytosine resistance, involving UMP pyrophosphorylase, present a significant clinical challenge.
    • Understanding these distinct resistance pathways is essential for developing new antifungal therapies.

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