eMedicine Specialties > Dermatology > Fungal Infections

Tinea Corporis: Treatment & Medication

Author: Mary Elizabeth Rushing Lott, MD, Senior Resident, Department of Pediatrics, Miami Children's Hospital
Coauthor(s): Gwendolyn Zember, MD, Consulting Staff, Department of Internal Medicine, University Hospital; Jack L Lesher Jr, MD, Chief, Professor, Department of Internal Medicine, Section of Dermatology, Medical College of Georgia
Contributor Information and Disclosures

Updated: Jun 5, 2008

Treatment

Medical Care

Topical therapy is recommended for a localized infection because dermatophytes rarely invade living tissues. Topical therapy should be applied to the lesion and at least 2 cm beyond this area once or twice a day for at least 2 weeks, depending on which agent is used. Topical azoles and allylamines show high rates of clinical efficacy. These agents inhibit the synthesis of ergosterol, a major fungal cell membrane sterol. 

• The topical azoles (eg, econazole, ketoconazole, clotrimazole, miconazole, oxiconazole, sulconazole, sertaconazole) inhibit the enzyme lanosterol 14-alpha-demethylase, a cytochrome P-450–dependent enzyme that converts lanosterol to ergosterol. Inhibition of this enzyme results in unstable fungal cell membranes and causes membrane leakage. The weakened dermatophyte is unable to reproduce and is slowly killed by fungistatic action. Sertaconazole nitrate is one of the newest topical azoles. It has fungicidal and anti-inflammatory abilities and is used as a broad-spectrum agent. It may have a reservoir effect and therefore is a good choice for noncompliant patients. Lastly, Liebel et al published in vitro data in 2006, reporting this drug has anti-itch properties.⁸
• Allylamines (eg, naftifine, terbinafine) and the related benzylamine butenafine inhibit squalene epoxidase, which converts squalene to ergosterol. Inhibition of this enzyme causes squalene, a substance toxic to fungal cells, to accumulate intracellularly and leads to rapid cell death. Allylamines bind effectively to the stratum corneum because of their lipophilic nature. They also penetrate deeply into hair follicles.⁹
• Ciclopirox olamine is a topical fungicidal agent. It causes membrane instability by accumulating inside fungal cells and interfering with amino acid transport across the fungal cell membrane.
• A low-to-medium potency topical corticosteroid can be added to the topical antifungal regimen to relieve symptoms. The steroid can provide rapid relief from the inflammatory component of the infection, but the steroid should only be applied for the first few days of treatment. Prolonged use of steroids can lead to persistent and recurrent infections, longer duration of treatment regimens, and adverse effects of skin atrophy, striae, and telangiectasias.

Systemic therapy may be indicated for tinea corporis that includes extensive skin infection, immunosuppression, resistance to topical antifungal therapy, and comorbidities of tinea capitis or tinea unguium. Use of oral agents requires attention to potential drug interactions and monitoring for adverse effects.

• The mechanism of action or oral micronized griseofulvin against dermatophytes is disruption of the microtubule mitotic spindle formation in metaphase, causing arrest of fungal cell mitosis. A dose of 10 mg/kg/d for 4 weeks is effective. In addition, griseofulvin induces the cytochrome P-450 enzyme system and can increase the metabolism of CYP-450–dependent drugs. It is the systemic drug of choice for tinea corporis infections in children.
• Systemic azoles (eg, fluconazole, itraconazole, ketoconazole) function similar to the topical agents, causing cell membrane destruction.⁹
  • Oral ketoconazole at 3-4 mg/kg/d may be given. However, this agent carries an associated risk of hepatitis in less than 1 in 10,000 cases and now is seldom used orally for dermatophyte infections.
  • Fluconazole at 50-100 mg/d or 150 mg once weekly for 2-4 weeks is used with good results.
  • Oral itraconazole in doses of 100 mg/d for 2 weeks shows high efficacy. With an increased dose of 200 mg/d, the treatment duration can be reduced to 1 week. However, the cytochrome P-450 activity of itraconazole allows for potential interactions with other commonly prescribed drugs.
  • Based on E-test for susceptibility of T rubrum, voriconazole was the most active and fluconazole was the least active of the azole drugs.¹⁰
• Oral terbinafine may be used at a dosage of 250 mg/d for 2 weeks; the potential exists for cytochrome P-450, specifically CYP-2D6, drug interactions with this agent.
• Systemic therapy is needed when the infection involves hair follicles, such as Majocchi granuloma. In this case, topical therapy may serve as adjunct treatment with the oral medication. 
• The preferred treatment for tinea imbricata is griseofulvin or terbinafine, although some resistance has developed to oral griseofulvin.¹¹

Surgical Care

Surgical treatment is usually not indicated except for drainage of superficial vesicles, bullae, pustules, or deep abscesses.

Medication

The goals of pharmacotherapy are to reduce morbidity and to prevent complications. Topical antifungal agents are effective for treating most cases of tinea corporis. Systemic therapy may be indicated for tinea corporis that is extensive, involves immunocompromised patients, or is refractory to topical therapy. For severe infections, systemic therapy can be combined with topical antifungal treatments.

Topical allylamines

Naftifine 1% cream or gel (Naftin)

Broad-spectrum antifungal agent that appears to interfere with sterol biosynthesis by inhibiting the enzyme squalene 2,3-epoxidase. This inhibition results in decreased amounts of sterols, causing cell death. If no clinical improvement occurs after 4 wk, reevaluate patient.

Terbinafine 1% cream (Lamisil)

Fungicidal activity; synthetic allylamine derivative that inhibits squalene epoxidase, a key enzyme in sterol biosynthesis of fungi, resulting in deficiency in ergosterol that causes fungal cell death. Use until symptoms significantly improve.

Topical pyridones

Ciclopirox olamine 1% cream (Loprox)

Interferes with synthesis of DNA, RNA, and protein by inhibiting transport of essential elements in fungal cells.

Topical benzylamines

Butenafine 1% cream (Mentax)

Inhibits squalene epoxidation, which, in turn, causes blockage of ergosterol biosynthesis (an essential component of fungal cell membranes), causing fungal cell growth to arrest.

Systemic azoles

Fluconazole (Diflucan)

Synthetic oral antifungal (broad-spectrum bistriazole) that selectively inhibits fungal cytochrome P-450 and sterol C-14 alpha-demethylation, which prevents conversion of lanosterol to ergosterol, thereby disrupting cellular membranes. Has little affinity for mammalian cytochromes, which is believed to explain its low toxicity. Available as tab for oral administration, as powder for oral susp, and as a sterile solution for IV use. Has fewer adverse effects and better tissue distribution than older systemic imidazoles.

Itraconazole (Sporanox)

Fungistatic activity; synthetic triazole antifungal agent that inhibits fungal cell growth by inhibiting the cytochrome P-450–dependent synthesis of ergosterol, a vital component of fungal cell membranes.

Ketoconazole (Nizoral)

Inhibits synthesis of ergosterol (main sterol of fungal cell membranes), causing cellular components to leak; results in cell death.

Systemic allylamines

Terbinafine (Lamisil, Daskil)

Fungicidal activity; synthetic allylamine derivative that inhibits squalene epoxidase, a key enzyme in sterol biosynthesis of fungi, resulting in a deficiency in ergosterol that causes fungal cell death. Use until symptoms significantly improve.

Other systemic antifungals

Griseofulvin (Fulvicin)

Fungistatic activity; fungal cell division is impaired by interfering with microtubule. Binds to keratin precursor cells. Keratin is gradually replaced by noninfected tissue, which is highly resistant to fungal invasions.

Topical azoles

Clotrimazole 1% cream (Mycelex, Lotrimin)

Nonabsorbable imidazole. Broad-spectrum synthetic antifungal agent that inhibits growth of fungus by altering cell membrane permeability, which causes fungal cell death.
Therapy is directed at the underlying condition, with the goal of minimizing symptoms and preventing complications.

Ketoconazole 2% cream (Nizoral)

Imidazole, broad-spectrum antifungal agent indicated for topical treatment of tinea corporis. Inhibits synthesis of ergosterol (main sterol of fungal cell membranes), causing cellular components to leak; result is cell death.

Miconazole 2% cream or lotion (Monistat)

Damages fungal cell-wall membrane by inhibiting biosynthesis of ergosterol. Membrane permeability is increased, causing nutrients to leak and resulting in fungal cell death. Lotion is preferred in intertriginous areas. If cream is used, apply sparingly to avoid maceration effects.

Oxiconazole 1% cream (Oxistat)

Damages fungal cell wall membrane by inhibiting biosynthesis of ergosterol. Membrane permeability is increased, causing nutrients to leak, resulting in fungal cell death.

Sertaconazole 2% cream (Ertaczo)

Topical imidazole antifungal active against T rubrum, T mentagrophytes, and Epidermophyton floccosum.

Sulconazole 1% cream or solution (Exelderm)

Broad-spectrum antifungal agent that inhibits synthesis of ergosterol, causing cellular components to leak and resulting in fungal cell death.

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