eMedicine Specialties > Dermatology > Fungal Infections

Tinea Corporis

Author: Jack L Lesher Jr, MD, Chief, Professor, Department of Internal Medicine, Section of Dermatology, Medical College of Georgia
Contributor Information and Disclosures

Updated: Dec 2, 2009

Introduction

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.1 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. 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.2

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%).3

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.

Clinical

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.
    • Tinea corporis gladiatorum is a dermatophyte infection spread by skin-to-skin contact between wrestlers.4,5
    • 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.6
    • Tinea incognito is tinea corporis with an altered, nonclassic presentation due to corticosteroid treatment.7

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, as shown in the image below.

    • Large, erythematous, scaly plaque.

      Large, erythematous, scaly plaque.

      Large, erythematous, scaly plaque.

      Large, erythematous, scaly plaque.

    • Following central resolution, the lesion may become annular in shape, as is shown in the image below.

    • Annular plaque.

      Annular plaque.

      Annular plaque.

      Annular plaque.

    • As a result of the inflammation, scale, crust, papules, vesicles, and even bullae can develop, especially in the advancing border.8
    • Rarely, tinea corporis can present as purpuric macules, called tinea corporis purpurica.9 One report describes 2 cases of tinea corporis purpurica resulting from self-inoculation with Trichophyton violaceum.10
    • 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,7,11 Trichophyton interdigitale, Trichophyton verrucosum,12 Microsporum canis, and Microsporum gypseum6 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.11
    • 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.

More on Tinea Corporis

Overview: Tinea Corporis
Differential Diagnoses & Workup: Tinea Corporis
Treatment & Medication: Tinea Corporis
Follow-up: Tinea Corporis
Multimedia: Tinea Corporis
References

References

  1. Foster KW, Ghannoum MA, Elewski BE. Epidemiologic surveillance of cutaneous fungal infection in the United States from 1999 to 2002. J Am Acad Dermatol. May 2004;50(5):748-52. [Medline].

  2. Seyfarth F, Goetze S, Erhard M, Burmester A, Elsner P, Hipler UC. [Infection with a rare geophilic dermatophyte.]. Hautarzt. Aug 14 2009;[Medline].

  3. Yehia MA, El-Ammawi TS, Al-Mazidi KM, Abu El-Ela MA, Al-Ajmi HS. The Spectrum of Fungal Infections with a Special Reference to Dermatophytoses in the Capital Area of Kuwait During 2000-2005: A Retrospective Analysis. Mycopathologia. Nov 17 2009;[Medline].

  4. Adams BB. Tinea corporis gladiatorum. J Am Acad Dermatol. Aug 2002;47(2):286-90. [Medline].

  5. Ilkit M, Saracli M, Kurdak H, et al. Clonal outbreak of Trichophyton tonsurans tinea capitis gladiatorum among wrestlers in Adana, Turkey. Med Mycol. Oct 14 2009;[Medline].

  6. Sun PL, Ho HT. Concentric rings: an unusual presentation of tinea corporis caused by Microsporum gypseum. Mycoses. Mar 2006;49(2):150-1. [Medline].

  7. Sanchez-Castellanos ME, Mayorga-Rodriguez JA, Sandoval-Tress C, Hernandez-Torres M. Tinea incognito due to Trichophyton mentagrophytes. Mycoses. Jan 2007;50(1):85-7. [Medline].

  8. Ziemer M, Seyfarth F, Elsner P, Hipler UC. Atypical manifestations of tinea corporis. Mycoses. 2007;50 Suppl 2:31-5. [Medline].

  9. Kim HS, Cho BK, Oh ST. A case of tinea corporis purpurica. Mycoses. Jul 2007;50(4):314-6. [Medline].

  10. Romano C, Massai L, Strangi R, Feci L, Miracco C, Fimiani M. Tinea corporis purpurica and onychomycosis caused by Trichophyton violaceum. Mycoses. Sep 22 2009;[Medline].

  11. Shiraki Y, Hiruma M, Matsuba Y, 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].

  12. Placzek M, van den Heuvel ME, Flaig MJ, Korting HC. Perniosis-like tinea corporis caused by Trichophyton verrucosum in cold-exposed individuals. Mycoses. Nov 2006;49(6):476-9. [Medline].

  13. Seyfarth F, Ziemer M, Gräser Y, Elsner P, Hipler UC. Widespread tinea corporis caused by Trichophyton rubrum with non-typical cultural characteristics--diagnosis via PCR. Mycoses. 2007;50 Suppl 2:26-30. [Medline].

  14. Weinstein A, Berman B. Topical treatment of common superficial tinea infections. Am Fam Physician. May 15 2002;65(10):2095-102. [Medline].

  15. 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].

  16. Leyden J. Pharmacokinetics and pharmacology of terbinafine and itraconazole. J Am Acad Dermatol. May 1998;38(5 Pt 3):S42-7. [Medline].

  17. da Silva Barros ME, de Assis Santos D, Soares Hamdan J. Antifungal susceptibility testing of Trichophyton rubrum by E-test. Arch Dermatol Res. May 2007;299(2):107-9. [Medline].

  18. 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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  21. [Guideline] Drake LA, Dinehart SM, Farmer ER, et al. Guidelines of care for superficial mycotic infections of the skin: tinea corporis, tinea cruris, tinea faciei, tinea manuum, and tinea pedis. Guidelines/Outcomes Committee. American Academy of Dermatology. J Am Acad Dermatol. Feb 1996;34(2 Pt 1):282-6. [Medline].

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  24. Lesher JL. Therapeutic agents for dermatologic fungal diseases. In: Elewski BE, ed. Cutaneous Fungal Infections. Malden: Blackwell Science; 1998:321-46.

  25. 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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Further Reading

Keywords

tinea corporis, ringworm, dermatophyte infection, Trichophyton species, Microsporum species, Epidermophyton species, Trichophyton rubrum, T rubrum, Microsporum canis, M canis, Trichophyton mentagrophytes, T mentagrophytes, Trichophyton tonsurans, T tonsurans, Trichophyton concentricum, T concentricum, Majocchi granuloma, Majocchi's granuloma, tinea imbricata, tinea capitis

Contributor Information and Disclosures

Author

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 Dermatological Association, American Medical Association, American Society for Dermatologic Surgery, Medical Association of Georgia, Society for Investigative Dermatology, and Southern Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Janet Fairley, MD, Professor and Head, Department of Dermatology, University of Iowa
Janet Fairley, MD is a member of the following medical societies: American Academy of Dermatology, American Dermatological Association, American Federation for Medical Research, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

Pharmacy Editor

Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University 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, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Rosalie Elenitsas, MD, Herman Beerman Associate 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 and American Society of Dermatopathology
Disclosure: Nothing to disclose.

CME Editor

Joel M Gelfand, MD, MSCE, Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania
Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology
Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds Investigator; Genentech Grant/research funds investigator; Centocor Consulting fee Consulting; Abbott Grant/research funds investigator; Abbott Consulting fee Consulting; Novartis  investigator; Pfizer Grant/research funds investigator; Celgene Consulting fee DMC Chair; NIAMS and NHLBI Grant/research funds investigator

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
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