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Tinea Corporis

  • Author: Jack L Lesher, Jr, MD; Chief Editor: Dirk M Elston, MD  more...
Updated: Nov 17, 2015

Practice Essentials

Tinea corporis is a superficial dermatophyte infection characterized by either inflammatory or noninflammatory lesions on the glabrous skin (ie, skin regions other than the scalp, groin, palms, and soles).[1] Three anamorphic (asexual or imperfect) genera cause dermatophytoses: Trichophyton, Microsporum, and Epidermophyton. Dermatophytes may infect humans (anthropophilic) or nonhuman mammals (zoophilic), or they may reside primarily in the soil (geophilic).

Signs and symptoms

Tinea corporis can manifest as follows:

  • Typically, the lesion begins as an erythematous, scaly plaque that may rapidly worsen (see the image below)
    Large, erythematous, scaly plaque. Large, erythematous, scaly plaque.
  • Following central resolution, the lesion may become annular in shape (see the image below)
    Annular plaque. Annular plaque.
  • The inflammation can cause scale, crust, papules, vesicles, and even bullae to develop, especially in the advancing border
  • Rarely, tinea corporis can present as purpuric macules

Infections due to zoophilic or geophilic dermatophytes may produce a more intense inflammatory response than those caused by anthropophilic microbes

Patients who are immunocompromised or infected with the human immunodeficiency virus (HIV) often have atypical presentations, including deep abscesses or a disseminated skin infection.

Majocchi granuloma

This variant of tinea corporis is a fungal infection of the hair, hair follicles, and, often, surrounding dermis. Typically caused by Trichophyton rubrum, it manifests as perifollicular, granulomatous nodules typically in a distinct location, which is the lower two thirds of the leg in females, with an associated granulomatous reaction. Majocchi granuloma often occurs in females who shave their legs.

Tinea corporis gladiatorum

This variant is a dermatophyte infection spread by skin-to-skin contact between wrestlers;[2, 3] it often manifests on the head, neck, and arms, which is a distribution consistent with the areas of contact in wrestling.

Tinea imbricata

Another variant of tinea corporis, this form is found mainly in Southeast Asia, the South Pacific, Central America, and South America. Tinea imbricata is caused by T concentricum[4] and is recognized clinically by its distinct, scaly plaques arranged in concentric rings.

Tinea incognito

This is tinea corporis with an altered, nonclassic presentation due to corticosteroid treatment.[5]

See Clinical Presentation for more detail.


Laboratory studies

A potassium hydroxide (KOH) examination of skin scrapings, used to visualize fungal elements removed from the skin's stratum corneum, may be diagnostic in tinea corporis.

A fungal culture, which is often used as an adjunct to KOH for diagnosis, is more specific than KOH for detecting a dermatophyte infection. Therefore, if the clinical suspicion is high yet the KOH result is negative, a fungal culture should be obtained.

If the above clinical evaluations are inconclusive, a polymerase chain reaction (PCR) assay for fungal deoxyribonucleic acid (DNA) identification can be used.[6]

For atypical presentations of tinea corporis, further evaluation for HIV infection and/or an immunocompromised state should be considered.


A skin biopsy with a hematoxylin and eosin staining of tinea corporis demonstrates spongiosis, parakeratosis, and a superficial inflammatory infiltrate. Neutrophils may be seen in the stratum corneum, which is a significant diagnostic clue. On occasion, septate branching hyphae are seen in the stratum corneum with hematoxylin and eosin stain, but special fungal stains (eg, periodic acid-Schiff, Gomori methenamine silver) may be required.

See Workup for more detail.


Topical therapy is recommended for a localized infection because dermatophytes rarely invade living tissues. 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 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.

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.[7]

Systemic therapy may be indicated if tinea corporis includes extensive skin infection, immunosuppression, resistance to topical antifungal therapy, or the comorbid presence of tinea capitis or tinea unguium.

See Treatment and Medication for more detail.



Tinea corporis is a superficial dermatophyte infection characterized by either inflammatory or noninflammatory lesions on the glabrous skin (ie, skin regions except the scalp, groin, palms, and soles). Three anamorphic (asexual or imperfect) genera cause dermatophytoses: Trichophyton, Microsporum, and Epidermophyton. Dermatophytes may infect humans (anthropophilic), infect nonhuman mammals (zoophilic), or reside primarily in the soil (geophilic).



Dermatophytes preferentially inhabit the nonliving, cornified layers of the skin, hair, and nail, which is attractive for its warm, moist environment conducive to fungal proliferation. Fungi may release keratinases and other enzymes to invade deeper into the stratum corneum, although typically the depth of infection is limited to the epidermis and, at times, its appendages. They generally do not invade deeply, owing to nonspecific host defense mechanisms that can include the activation of serum inhibitory factor, complement, and polymorphonuclear leukocytes.

Following the incubation period of 1-3 weeks, dermatophytes invade peripherally in a centrifugal pattern. In response to the infection, the active border has an increased epidermal cell proliferation with resultant scaling. This creates a partial defense by way of shedding the infected skin and leaving new, healthy skin central to the advancing lesion. Elimination of dermatophytes is achieved by cell-mediated immunity.

Trichophyton rubrum is a common dermatophyte and, because of its cell wall, is resistant to eradication. This protective barrier contains mannan, which may inhibit cell-mediated immunity, hinder the proliferation of keratinocytes, and enhance the organism's resistance to the skin's natural defenses.[8]




Tinea corporis is a common infection more often seen in typically hot, humid climates. T rubrum is the most common infectious agent in the world and is the source of 47% of tinea corporis cases.[9, 10] Trichophyton tonsurans is the most common dermatophyte to cause tinea capitis, and people with an anthropophilic tinea capitis infection are more likely to develop associated tinea corporis. Therefore, the prevalence of tinea corporis caused by T tonsurans is increasing.[11] Microsporum canis is the third most common causative organism and associated with 14% of tinea corporis infections. A rare case of Microsporum fulvum skin infection (forearm) has recently been reported, identified by ITS sequencing and mass spectrometry.[12]

A 5-year study from Kuwait that included 2730 patients reported that fungal skin infections remain prevalent in that country, specifically the Capital area. In those patients with dermatophytes, 6 species were isolated. They included Trichophyton mentagrophytes (39%), M canis (16%), T rubrum (10%), Epidermophyton floccosum (6.2%), Trichophyton violaceum (2.4%), and Trichophyton verrucosum (0.4%).[13]


Tinea corporis occurs in both men and women. Women of childbearing age are more likely to develop tinea corporis as a result of their greater frequency of contact with infected children.


Tinea corporis affects persons of all age groups, but prevalence is highest in preadolescents. Tinea corporis acquired from animals is more common in children. Tinea corporis secondary to tinea capitis typically occurs in children because tinea capitis is more common in this population.

Contributor Information and Disclosures

Jack L Lesher, Jr, MD Chief, Professor, Department of Internal Medicine, Section of Dermatology, Medical College of Georgia

Jack L Lesher, Jr, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, Medical Association of Georgia, Society for Investigative Dermatology, Southern Medical Association

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.

Rosalie Elenitsas, MD Herman Beerman Professor of Dermatology, University of Pennsylvania School of Medicine; Director, Penn Cutaneous Pathology Services, Department of Dermatology, University of Pennsylvania Health System

Rosalie Elenitsas, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, American Society of Dermatopathology, Pennsylvania Academy of Dermatology

Disclosure: Received royalty from Lippincott Williams Wilkins for textbook editor.

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

Janet Fairley, MD Professor and Head, Department of Dermatology, University of Iowa, Roy J and Lucille A Carver College of Medicine

Janet Fairley, MD is a member of the following medical societies: American Academy of Dermatology, American Federation for Medical Research, Society for Investigative Dermatology

Disclosure: Nothing to disclose.


The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors Mary Elizabeth Rushing Lott, MD and Gwendolyn Zember, MD, to the development and writing of this article.

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Annular plaque.
Large, erythematous, scaly plaque.
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