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Systemic candidiasis in mice treated with prednisolone and amphotericin B. 2. Ultrastructure and evidence for fungal

W Blyth, G E Stewart

    Mycopathologia
    |December 29, 1978
    PubMed

    Insights

    Amphotericin B (AmB) causes ultrastructural damage to Candida albicans cells, including cell wall changes and organelle destruction. Toxic protein components were detected in AmB-treated fungal extracts, impacting mice treated with Actinomycin D.

    Area of Science:

    • Mycology
    • Cell Biology
    • Pharmacology

    Background:

    • Candida albicans is a common fungal pathogen.
    • Amphotericin B (AmB) is a key antifungal agent.
    • Prednisolone can modulate host response to infection.

    Purpose of the Study:

    • To investigate the ultrastructural effects of Amphotericin B on Candida albicans cells.
    • To assess the toxicity of Amphotericin B-treated Candida albicans extracts.
    • To determine the influence of prednisolone on these effects.

    Main Methods:

    • Transmission electron microscopy to observe cellular ultrastructure.
    • In vitro and in vivo treatment of Candida albicans with Amphotericin B.
    • Administration of fungal extracts and leachates to mice, with or without Actinomycin D.
    • Polyacrylamide gel electrophoresis to analyze toxic components.

    Main Results:

    • Amphotericin B induced plasmolysis, vacuolation, and organelle destruction in Candida albicans.
    • Cell wall lamination was prominent in vivo, particularly with prednisolone co-treatment.
    • Somatic extracts and leachates from treated cells exhibited low-grade toxicity in mice.
    • Toxic components were identified as high molecular weight proteins.

    Conclusions:

    • Amphotericin B causes significant cellular damage to Candida albicans.
    • Prednisolone may enhance the in vivo effects of Amphotericin B on fungal cell walls.
    • Fungal extracts from Amphotericin B treatment contain toxic, proteinaceous components.

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