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Cutaneous Candidiasis Medication

  • Author: Noah S Scheinfeld, JD, MD, FAAD; Chief Editor: Dirk M Elston, MD  more...
 
Updated: Feb 05, 2016
 

Medication Summary

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.[42]

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.[43]

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Antifungal agents

Class Summary

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 (Mycostatin)

 

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 topical (Micatin, Monistat-Derm, Monistat)

 

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 (Lotrimin, Mycelex, Gyne-Lotrimin)

 

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 (Diflucan)

 

Fluconazole is a synthetic oral antifungal (broad-spectrum bistriazole) that selectively inhibits fungal cytochrome P-450 and sterol C-14 alpha-demethylation.

Itraconazole (Sporanox)

 

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 (Lamisil)

 

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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Contributor Information and Disclosures
Author

Noah S Scheinfeld, JD, MD, FAAD Assistant Clinical Professor, Department of Dermatology, Weil Cornell Medical College; Consulting Staff, Department of Dermatology, St Luke's Roosevelt Hospital Center, Beth Israel Medical Center, New York Eye and Ear Infirmary; Assistant Attending Dermatologist, New York Presbyterian Hospital; Assistant Attending Dermatologist, Lenox Hill Hospital, North Shore-LIJ Health System; Private Practice

Noah S Scheinfeld, JD, MD, FAAD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Abbvie<br/>Received income in an amount equal to or greater than $250 from: Optigenex<br/>Received salary from Optigenex for employment.

Coauthor(s)

Matthew C Lambiase, DO Dermatologist, Skin Cancer and Dermatology Institute, Reno, NV

Disclosure: Nothing to disclose.

Specialty Editor Board

Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Texas Medical Association, Association of Military Dermatologists, Texas Dermatological Society

Disclosure: Nothing to disclose.

Paul Krusinski, MD Director of Dermatology, Fletcher Allen Health Care; Professor, Department of Internal Medicine, University of Vermont College of Medicine

Paul Krusinski, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Franklin Flowers, MD Department of Dermatology, Professor Emeritus Affiliate Associate Professor of Pathology, University of Florida College of Medicine

Franklin Flowers, MD is a member of the following medical societies: American College of Mohs Surgery

Disclosure: Nothing to disclose.

Acknowledgements

Jessica M Allan, MD Private Practice

Disclosure: Nothing to disclose.

Daniel S Lehman, MD Fellow in Minimally Invasive Urology/Oncology, Department of Urology, Columbia University Medical Center

Disclosure: Nothing to disclose.

Thomas K Vaughan, MD Assistant Chief, Dermatology Service, Madigan Army Medical Center

Disclosure: Nothing to disclose.

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A moist, erosive, pruritic patch of the perianal skin and perineum (with satellite pustule formation) is demonstrated in this woman with extensive candidosis.
Discrete superficial pustules developed within hours of birth on the hand of an otherwise healthy newborn. A potassium hydroxide preparation revealed spores and pseudomycelium, and culture demonstrated the presence of Candida albicans.
Dry, red, superficially scaly, pruritic macules and patches on the penis represent candidal balanitis.
White plaques are present on the buccal mucosa and the undersurface of the tongue and represent thrush. When wiped off, the plaques leave red erosive areas.
Erythema, maceration, and satellite pustules in the axilla, accompanied by soreness and pruritus result in a form of intertrigo.
A nailfold with candidal infection becomes erythematous, swollen, and tender with an occasional discharge
Soreness and cracks at the lateral angles of the mouth (angular cheilitis) is a frequent expression of candidosis in elderly individuals.
Fine superficial pustules on an erythematous patchy base are suggestive of candidosis.
Candida infection should be in the differential diagnosis when one or more nails become discolored, has subungual discoloration, nailplate separation from the nailbed, and lack evidence of a dermatophyte.
Candidiasis. Courtesy of Hon Pak, MD.
 
 
 
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