AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Acknowledgments
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Acknowledgments
• Multimedia
• References

Background

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).

Pathophysiology

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.

Frequency

International

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. 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 (see Tinea Capitis). Therefore, the prevalence of tinea corporis caused by T tonsurans is increasing. Microsporum canis is the third most common causative organism and associated with 14% of tinea corporis infections.

Mortality/Morbidity

Dermatophyte infections do not result in significant mortality, but they can greatly affect quality of life.

Sex

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.

Age

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.

The Medscape Pediatric Dermatology Resource Center may be of interest.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Acknowledgments
• Multimedia
• References

History

Symptoms, contact history, recent travel, and international residence are relevant clues in the history of a person with tinea corporis.

• Infected patients may have variable symptoms.  
• • Patients can be asymptomatic.
  • A pruritic, annular plaque is characteristic of a symptomatic infection. Patients occasionally can experience a burning sensation.
  • HIV-positive or immunocompromised patients may develop severe pruritus or pain.
• Tinea corporis may result from contact with infected humans, animals, or inanimate objects. The history may include occupational (eg, farm worker, zookeeper, laboratory worker, veterinarian), environmental (eg, gardening, contact with animals), or recreational (eg, contact sports, contact with sports facilities) exposure.
• A few clinical variants are described, with distinct presentations.  
• • Majocchi granuloma, typically caused by T rubrum, is a fungal infection in hair, hair follicles, and, often, the surrounding dermis, with an associated granulomatous reaction. Majocchi granuloma often occurs in females who shave their legs. See Majocchi Granuloma.
  • Tinea corporis gladiatorum is a dermatophyte infection spread by skin-to-skin contact between wrestlers.¹
  • Tinea imbricata is a form of tinea corporis found mainly in Southeast Asia, the South Pacific, Central America, and South America. It is caused by Trichophyton concentricum.²
  • Tinea incognito is tinea corporis with an altered, nonclassic presentation due to corticosteroid treatment.³

Physical

• Tinea corporis can manifest in a variety of ways.  
• • Typically, the lesion begins as an erythematous, scaly plaque that may rapidly worsen and enlarge.
  • Following central resolution, the lesion may become annular in shape.
  • As a result of the inflammation, scale, crust, papules, vesicles, and even bullae can develop, especially in the advancing border.
  • Rarely, it can present as purpuric macules, called tinea corporis purpurica.⁴
  • Infections due to zoophilic or geophilic dermatophytes may produce a more intense inflammatory response than those caused by anthropophilic microbes.
  • HIV-infected or immunocompromised patients often have atypical presentations including deep abscesses or a disseminated skin infection.
• Majocchi granuloma manifests as perifollicular, granulomatous nodules typically in a distinct location, which is the lower two thirds of the leg in females.
• Tinea corporis gladiatorum often manifests on the head, neck, and arms, which is a distribution consistent with the areas of skin-to-skin contact in wrestling.
• Tinea imbricata is recognized clinically by its distinct scaly plaques arranged in concentric rings.

Causes

• Tinea corporis can be caused by a variety of dermatophytes, although prevalence and patient history are very helpful in identifying the most likely organism.  
• • Internationally, the most common cause is T rubrum.
  • T tonsurans, Trichophyton mentagrophytes,^{3, 5} Trichophyton interdigitale, Trichophyton verrucosum,⁶ Microsporum canis, and Microsporum gypseum² are also known to produce infection.
  • Tinea imbricata is caused by Trichophyton concentricum.
• Dermatophytoses may be acquired from different sources, such as people, animals, or soil.  
• • Infected humans are the most common source of tinea corporis in the United States.
  • Contact with contaminated household pets, farm animals, and fomites (eg hair brushes, towels) can spread infection. 
  • T verrucosum causes 98% of dermatophyte infections in cattle and is showing increasing prevalence of infection in human contacts. 
  • T mentagrophytes is spread by rabbits, guinea pigs, and small rodents.⁵
  • Infection with M gypseum, a geophilic organism, can mimic tinea imbricata in presentation.
• Because fungal arthroconidia can survive in the environment, recurrent outbreaks may occur.

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Acknowledgments
• Multimedia
• References

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Acknowledgments
• Multimedia
• References

Lab Studies

• A potassium hydroxide (KOH) examination of skin scrapings may be diagnostic.  
• • A KOH test is a microscopic preparation used to visualize fungal elements removed from the skin's stratum corneum.
  • The sample should be taken from the active border of a lesion because this region provides the highest yield of fungal elements. A KOH preparation from a vesicular lesion should be made from the roof of the vesicle.
  • The KOH helps dissolve the keratin and leaves fungal elements intact, revealing numerous septate, branching hyphae amongst epithelial cells.
  • A counterstain, such as chlorazol black E or Parker blue-black ink, may help visualize hyphae under the microscope.
• A fungal culture is often used as an adjunct to KOH for diagnosis. Fungal culture 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.
• A few culture mediums are available for dermatophyte growth.  
• • Sabouraud agar containing neopeptone or polypeptone agar and glucose is often used for fungal culture. However, it does not contain antibiotics and may allow overgrowth of fungal and bacterial contaminants.
  • Mycosel, a commonly used agar, is similar to Sabouraud agar but has antibiotics.
  • Commonly, dermatophyte test medium (DTM) is used. It contains antibacterial (ie, gentamicin, chlortetracycline) and antifungal (ie, cycloheximide) solutions in a nutrient agar base. This combination isolates dermatophytes while suppressing other fungal and bacterial species that may contaminate the culture.
• Following culture inoculation, potential fungal growth is monitored for 2 weeks.
• Positive culture results vary depending on the medium used.  
• • DTM contains phenol red solution, which causes a color change from straw-yellow to bright-red under alkaline conditions, indicating a positive dermatophyte culture result. However, the color makes identification of culture morphology (particularly pigmentation) difficult.
  • Sabouraud or Mycosel agar should be used to assess gross and microscopic colony characteristics.
• If the above clinical evaluations are inconclusive, the molecular method of polymerase chain reaction for fungal DNA identification can be applied.⁷ 
• For atypical presentations, further evaluation for HIV infection and/or an immunocompromised state should be considered.

Histologic Findings

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.

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Acknowledgments
• Multimedia
• References

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

Section 7 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Acknowledgments
• Multimedia
• References

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.

Drug Category: Topical allylamines

Drug Category: Topical pyridones

Drug Category: Topical benzylamines

Drug Category: Systemic azoles

Drug Category: Systemic allylamines

Drug Category: Other systemic antifungals

Drug Category: Topical azoles

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Acknowledgments
• Multimedia
• References

Further Outpatient Care

• Follow-up care should be determined per patient need, severity of infection, and response to treatment.

In/Out Patient Meds

• See Medication.

Deterrence/Prevention

• Imperative for preventing the spread of a dermatophyte infection is to discourage close contact between infected and noninfected individuals and to stop the sharing of fomites (eg, towels, hats, clothing).
• Because dermatophytes flourish in moist environments, patients should be advised to wear loose-fitting clothing made of cotton or synthetic materials.

Complications

• The infection may recur if therapy does not result in complete eradication of the organism, such as when patients stop applying topical therapy too soon or if the organism is resistant to the antifungal agent used.
• Reinfection may occur if a reservoir, such as an infected nail or hair follicle, is present. Many, if not most, adult patients with tinea corporis also have tinea pedis and unguium, which should be treated.

Prognosis

• For localized tinea corporis, the prognosis is excellent, with cure rates of 70-100% after treatment with topical azoles or allylamines or short-term or pulse systemic antifungals.

Patient Education

• For excellent patient education resources, visit eMedicine's Skin, Hair, and Nails Center. Also, see eMedicine's patient education article Ringworm on Body.

ACKNOWLEDGMENTS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Acknowledgments
• Multimedia
• References

The authors and editors of eMedicine gratefully acknowledge the contributions of previous Chief Editor, William James, MD, to the development and writing of this article.

MULTIMEDIA

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Acknowledgments
• Multimedia
• References

Media file 1:  Annular plaque.
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Media type:  Photo

Media file 2:  Large, erythematous, scaly plaque.
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Media type:  Photo

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Acknowledgments
• Multimedia
• References

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2. Sun PL, Ho HT. Concentric rings: an unusual presentation of tinea corporis caused by Microsporum gypseum. Mycoses. Mar 2006;49(2):150-1. [Medline].
3. Sánchez-Castellanos ME, Mayorga-Rodríguez JA, Sandoval-Tress C, Hernández-Torres M. Tinea incognito due to Trichophyton mentagrophytes. Mycoses. Jan 2007;50(1):85-7. [Medline].
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5. Shiraki Y, Hiruma M, Matsuba Y, Kano R, Makimura K, Ikeda S, et al. A case of tinea corporis caused by Arthroderma benhamiae (teleomorph of Tinea mentagrophytes) in a pet shop employee. J Am Acad Dermatol. Jul 2006;55(1):153-4. [Medline].
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8. Liebel F, Lyte P, Garay M, Babad J, Southall MD. Anti-inflammatory and anti-itch activity of sertaconazole nitrate. Arch Dermatol Res. Sep 2006;298(4):191-9. [Medline].
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11. Wingfield AB, Fernandez-Obregon AC, Wignall FS, Greer DL. Treatment of tinea imbricata: a randomized clinical trial using griseofulvin, terbinafine, itraconazole and fluconazole. Br J Dermatol. Jan 2004;150(1):119-26. [Medline].
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20. Lesher JL Jr. Oral therapy of common superficial fungal infections of the skin. J Am Acad Dermatol. Jun 1999;40(6 Pt 2):S31-4. [Medline].
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Article Last Updated: Jun 5, 2008