## Mechanism of Echinocandins **Key Point:** Echinocandins (caspofungin, micafungin, anidulafungin) are the only class of antifungals that target the fungal cell wall rather than the cell membrane or intracellular enzymes. ### Mechanism of Action Echinocandins inhibit **β-1,3-glucan synthase**, a fungal-specific enzyme responsible for synthesizing β-1,3-glucans — a critical structural component of the fungal cell wall. This leads to: 1. Disruption of cell wall integrity 2. Cell lysis and fungal death 3. Fungistatic or fungicidal activity depending on the organism ### Advantages Over Other Antifungals | Feature | Echinocandins | Amphotericin B | Azoles | Terbinafine | | --- | --- | --- | --- | --- | | **Target** | Cell wall | Cell membrane | Sterol synthesis | Ergosterol synthesis | | **Selectivity** | High (fungal-specific enzyme) | Moderate (mammalian sterols also affected) | Moderate | High | | **Nephrotoxicity** | Minimal | Severe | Minimal | Minimal | | **First-line for** | Invasive candidiasis, aspergillosis | Severe systemic infections | Cryptococcal meningitis, oral candidiasis | Dermatophyte infections | **High-Yield:** Echinocandins are the **preferred agents for invasive candidiasis** in hospitalized patients and are increasingly used for invasive aspergillosis, especially in neutropenic hosts. **Clinical Pearl:** Unlike azoles and amphotericin B, echinocandins do NOT penetrate the CNS well — they are NOT suitable for fungal meningitis. **Mnemonic:** **ECAM** — **E**chinocandins target **C**ell wall, **A**mphotericin targets **M**embrane.
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