Cutaneous Candidiasis Medication
- Author: Noah S Scheinfeld, JD, MD, FAAD; Chief Editor: Dirk M Elston, MD more...
The azoles are a group of synthetic antimycotic agents with a broad spectrum of activity. The primary drugs available include ketoconazole, miconazole, fluconazole, itraconazole, and econazole. The mechanism of action of azoles is blocking the synthesis of ergosterol, the primary sterol in the fungal cell membrane. The depletion of ergosterol alters the fluidity of the cell membrane and alters the action of the membrane-associated enzymes. This results in inhibition of replication and inhibition of the transformation of candidal yeast forms into hyphae, which is the invasive and pathogenic form of the parasite.
Nystatin and amphotericin are polyenes, which are active against some fungi but have little action on mammalian cells and no action on bacteria. They bind to cell membranes and interfere with permeability and transport functions. These antibiotics act as ionophores and causes leakage of cations.
Terbinafine is an allylamine that is fungicidal for a wide range of skin pathogens. It inhibits squalene epoxidase, which is involved in the synthesis of ergosterol from squalene in the fungal cell wall. The accumulation of squalene within the cell is toxic to the organism.
Naftifine (an allylamine antifungal) 2% cream, which is a stronger version of the older 1% cream, is a promising agent for hard-to-treat cutaneous candidal infections.
A case of chronic mucocutaneous candidosis that was cured with micafungin has been reported.
Voriconazole is another third-line treatment.
A stable nitric oxide (NO)–releasing nanoparticle (NO-np) system for treating cutaneous candidiasis has been proposed as a new treatment for extensive cutaneous candidiasis in burn patients.
Antifungal agents exert their fungicidal effect by altering the permeability of fungal cell membranes. The mechanism of action also may involve an alteration of RNA and DNA metabolism or an intracellular accumulation of peroxide toxic to the fungal cell.
Nystatin is a fungicidal and fungistatic antibiotic obtained from Streptomyces noursei. It is effective against various yeasts and yeastlike fungi. Nystatin changes permeability of the fungal cell membrane after binding to cell membrane sterols, causing cellular contents to leak.
Treatment should continue until 48 hours after the disappearance of symptoms.
Miconazole damages the fungal cell wall membrane by inhibiting the biosynthesis of ergosterol. Membrane permeability is increased, causing nutrients to leak out, resulting in fungal-cell death.
Lotion is preferred in intertriginous areas. If cream is used, apply sparingly to avoid maceration effects.
Clotrimazole is a broad-spectrum antifungal agent that inhibits yeast growth by altering cell membrane permeability, causing death of fungal cells. Reevaluate the diagnosis if no clinical improvement is seen after 4 weeks.
Fluconazole is a synthetic oral antifungal (broad-spectrum bistriazole) that selectively inhibits fungal cytochrome P-450 and sterol C-14 alpha-demethylation.
Itraconazole is a synthetic triazole antifungal agent that slows fungal cell growth by inhibiting cytochrome P-450–dependent synthesis of ergosterol, a vital component of fungal cell membranes.
Terbinafine is used for the treatment of paronychia; it is an allylamine antifungal, which inhibits squalene epoxidase and decreases ergosterol synthesis, causing fungal-cell death.
Use the medication until symptoms significantly improve. The duration of treatment should be longer than 1 week but not longer than 4 weeks. Terbinafine may not be as effective for candidal infections as azole antifungals.
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