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Questions and Answers
What is the primary mode of action of polyenes like Amphotericin B?
What is the primary mode of action of polyenes like Amphotericin B?
- Damage to cell wall synthesis
- Inhibition of RNA synthesis
- Inhibition of lanosterol conversion
- Disruption of cell membrane by binding to ergosterol (correct)
Which antifungal agent's resistance is associated with alterations in the FCY2, FCY1, and FUR genes?
Which antifungal agent's resistance is associated with alterations in the FCY2, FCY1, and FUR genes?
- Polyenes
- Antimetabolite (5-Fluorocytosine) (correct)
- Azole
- Echinocandins
What is the consequence of mutations in the genes responsible for glucan synthesis in fungi?
What is the consequence of mutations in the genes responsible for glucan synthesis in fungi?
- Enhanced protein synthesis
- Increased sensitivity to polyenes
- Inhibition of RNA synthesis
- Resistance to echinocandins (correct)
Which resistance mechanism is associated with the use of azole antifungals?
Which resistance mechanism is associated with the use of azole antifungals?
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What is a common resistance mechanism for polyenes?
What is a common resistance mechanism for polyenes?
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Study Notes
Polyenes
- Interrupt fungal cell membrane function by binding to ergosterol
- Amphotericin B, Nystatin, and Natamycin are examples
- Resistance mechanisms involve modifications in the fungi's membrane sterols, affecting genes like ERG3, ERG5, and ERG11
Antimetabolite (5-Fluorocytosine)
- Inhibits RNA and protein synthesis by binding 5-fluorouracil to the RNA strand
- Resistance develops through alterations in the FCY2, FCY1, and FUR genes that control flucytosine uptake and conversion
Azole
- Inhibits fungal lanosterol 14-demethyl ascytochrome
- Resistance occurs due to alterations and overexpression of ERG11, Cyp51A, and Cyp51B, encoding for lanosterol 14-alpha-demethylase enzyme
Echinocandins
- Inhibit 1,3-β-D-glucan synthase, essential for fungal cell wall synthesis
- Examples include Caspofungin, Micafungin, and Anidulafungin
- Resistance can arise from mutations in genes responsible for the glucan layer, such as FKS1 and FKS2
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