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Diagnosis: Tinea Corporis (commonly called 'Ringworm')

tinea corporis
Annular, scaling, pruritic rash

24 year old woman who developed an annular, scaling, pruritic rash on her arm 12 days after adopting a new cat.

Tinea Corporis, commonly called "Ringworm" (see interesting origin of name, below)

Definition

The key characteristic of Tinea corporis is that the fungus involves the glabrous (relatively hairless) skin. The infection is limited to the stratum corneum of the epidermis. Vellus hair (the fine hair present on glabrous skin) may be invaded, and the hair follicle may serve as a reservoir for the fungus.Tinea pedis, Tinea manuun, and Tinea cruris are referred to Tinea corporis that is limited to the foot, hand, and groin, respectively. There is otherwise little special about them. History lesson: The term tinea has an interesting origin. A worm of a moth would sometimes grow on a woolen blanket. The resulting round holes were similar to the rounded lesions seen on the skin of patients. The genus name for the moth was Tinea, and thus this name was used as part of the Latin binomials naming these infections.

Epidemiology

Transmission of tinea corporis may occur from direct contact with infected animals (especially cats and dogs), infected humans, or contaminated fomites such as furniture and clothing. Like many other fungal skin infections, warmth and humidity favor the occurrence of this infection. Therefore, tropical and subtropical regions have a higher incidence of tinea corporis [1320].

Tinea imbricata is an unusual form of Tinea corporis caused by T. concentricum. This form of Tinea is characterized by ring-like growth in overlapping circles that may have an autosomal dominant genetic predisposition [1724, 1915]. This may explain its geographic restriction to certain regions of the Far East, South Pacific, and South and Central America [310, 924].

Clinical manifestations

Tinea corporis can present on any area of the body. Zoophilic organisms commonly affect exposed areas like the face, neck and arms. Oppositely, anthropophilic organisms classically affect occluded areas of the skin or areas of trauma. In regards to the clinical appearance, multiple varieties have been described, and to make things a little more confusing, many of them have distinct names although they are all forms of tinea corporis![1320].

  • The classical and more common clinical variety in which annular lesions have active, erythematous and spreading borders with central clearing is called in common parlanceringworm and scientifically,tinea circinata. When herpetiform, subcorneal vesicles appear the term "bullous tinea corporis" has been used.
  • Between 3 to 4% of tinea corporis cases present with an erythematous, scaly rash on the face with or without telangiectasia, atrophy, and photoexacerbation. This clinical form, calledtinea fasciale, may be confused with lupus erythematosis [773, 1774].
  • When any of these dermatophytoses are treated with corticosteroids, the lesions take on an atypical appearance and lose the characteristic scaling of tinea corporis. Patches, papules, or small nodules appear. For this variety the termtinea incognito is used [1006].
  • Tinea profunda refers to the appearance of subcutaneous abscesses, which are frequently associated with T. mentagrophytes.
  • Tinea axillaris refers to the involvement of the axillary (armpit) region [193].
  • Other atypical inflammatory forms include the appearance of verrucous lesions, kerion-like lesions and/or nodular granulomas (Majocchi's granuloma).

    Prognosis and therapy

    Topical therapy is useful in cases of noninflammatory lesions. Systemic therapy with griseofulvin, terbinafine, ketoconazole, itraconazole or fluconazole is recommended for inflammatory varieties [565]. The following regimens are recommended:

    Drug

    Regimen

    Reference

    Griseofulvin

    500 mg once daily for 4-6 weeks

    [645]

    Fluconazole

    150 mg once daily for 4-6 weeks

    [645]

    Itraconazole

    100 mg daily for 1-2 weeks

    [1571]

    Terbinafine

    250 mg daily for 2-4 weeks

    [655]

    Histopathology

    Rarely is a biopsy required for the diagnosis of this condition. Classically, fungal elements are seen in the stratum corneum with PAS, silver methenamine or other fungal stain. If they are absent, pathology will show nonspecific lesions that resemble acute or chronic dermatitis [1320].

    Laboratory

    Direct examination

  • Superficial scraping from the spreading border of the lesion is recommended. If vesicular lesions predominate, the roof of the blister should be taken. These samples are mounted in 10% KOH and septate, branching hyphae with or without arthrospores should be seen.

    Isolation

  • Inoculate the clinical specimens onto Sabouraud glucose agar, incubate at 30°C and discard negative cultures in 4 weeks. For more details consult the chapters on the three species involved: Epidermophyton, Trichophyton, and Microsporum.

    Mycology (principal dermatophytes)

  • The three most common responsible for tinea corporis are:
  • Trichophyton rubrum
  • Microsporum canis
  • Trichophyton mentagrophytes

    However, other species implicated include:

  • Epidermophyton floccosum
  • Microsporum audouinii
  • Microsporum gypseum
  • Trichophyton megninii
  • Trichophyton schoenleinii
  • Trichophyton tonsurans
  • Trichophyton verrucosum

    Natural habitat

    Animals (stray cats and farm animals!) humans, soil

    Charles E. Crutchfield III, MD
    Clinical Adjunct Associate Professor of Dermatology
    At the
    University of Minnesota Medical School
    Medical Director, Crutchfield Dermatology
    www.CrutchfieldDermatology.com

    References

    193. Bell, S. A., M. Rocken, and H. C. Korting. 1996. Tinea axillaris, a variant of intertriginous tinea, due to non- occupational infection with Trichophyton verrucosum. Mycoses. 39:471-4.

    310. Budimulja, U., K. Kuswadji, S. Bramono, J. Basuki, L. S. Judanarso, S. Untung, S. Widagdo, Rohprabowo, Wydianto, D. Koesanto, and et al. 1994. A double-blind, randomized, stratified controlled study of the treatment of tinea imbricata with oral terbinafine or itraconazole. Br J Dermatol. 130 Suppl 43:29-31.

    489. De Keyser, P., M. De Backer, D. L. Massart, and K. J. Westelinck. 1994. Two-week oral treatment of tinea pedis, comparing terbinafine (250 mg/day) with itraconazole (100 mg/day): a double-blind, multicentre study. Br J Dermatol. 130 Suppl 43:22-5.

    565. Drake, L. A., S. M. Dinehart, E. R. Farmer, R. W. Goltz, G. F. Graham, M. K. Hordinsky, C. W. Lewis, D. M. Pariser, J. W. Skouge, S. B. Webster, D. C. Whitaker, B. Butler, B. J. Lowery, B. E. Elewski, M. L. Elgart, P. H. Jacobs, J. L. Lesher, Jr., and R. K. Scher. 1996. Guidelines of care for superficial mycotic infections of the skin: tinea capitis and tinea barbae. Guidelines/Outcomes Committee. American Academy of Dermatology. J Am Acad Dermatol. 34:290-4.

    645. Faergemann, J., N. J. Mork, A. Haglund, and T. Odegard. 1997. A multicentre (double-blind) comparative study to assess the safety and efficacy of fluconazole and griseofulvin in the treatment of tinea corporis and tinea cruris. Br J Dermatol. 136:575-7.

    655. Farag, A., M. Taha, and S. Halim. 1994. One-week therapy with oral terbinafine in cases of tinea cruris/corporis. Br J Dermatol. 131:684-6.

    773. Gilgor, R. S., J. P. Tindall, and M. Elson. 1971. Lupus-erythematosus-like tinea of the face (tinea faciale). JAMA. 215:2091-4.

    863. Gupta, A. K., P. D. Doncker, A. Heremans, P. Stoffels, G. E. Pierard, J. Decroix, M. Heenen, and H. Degreef. 1997. Itraconazole for the treatment of tinea pedis: a dosage of 400 mg/day given for 1 week is similar in efficacy to 100 or 200 mg/day given for 2 to 4 weeks. J Am Acad Dermatol. 36:789-92.

    923. Hay, R. J., J. M. McGregor, J. Wuite, K. S. Ryatt, C. Ziegler, and Y. M. Clayton. 1995. A comparison of 2 weeks of terbinafine 250 mg/day with 4 weeks of itraconazole 100 mg/day in plantar-type tinea pedis. Br J Dermatol. 132:604-8.

    924. Hay, R. J., S. Reid, E. Talwat, and K. Macnamara. 1984. Endemic tinea imbricata--a study on Goodenough Island, Papua New Guinea. Trans R Soc Trop Med Hyg. 78:246-51.

    1006. Ive, F. A., and R. Marks. 1968. Tinea incognito. Br Med J. 3:149-52.

    1207. Lesher, J. L., Jr. 1999. Oral therapy of common superficial fungal infections of the skin. J Am Acad Dermatol. 40:S31-4.

    1222. Leyden, J. J., and A. M. Kligman. 1978. Interdigital athlete's foot. The interaction of dermatophytes and resident bacteria. Arch Dermatol. 114:1466-72.

    1320. Martin, A. G., and G. S. Kobayashi. 1993. Fungal diseases with cutaneous involvement, p. 2421-2451. In T. B. Fitzpatrick (ed.), Dermatology in general medicine, vol. 2. McGraw-Hill, New York.

    1504. Nolting, S., and M. Brautigam. 1992. Clinical relevance of the antibacterial activity of terbinafine: a contralateral comparison between 1% terbinafine cream and 0.1% gentamicin sulphate cream in pyoderma. Br J Dermatol. 126 Suppl 39:56-60.

    1571. Pariser, D. M., R. J. Pariser, G. Ruoff, and T. L. Ray. 1994. Double-blind comparison of itraconazole and placebo in the treatment of tinea corporis and tinea cruris. J Am Acad Dermatol. 31:232-4.

    1639. Philpot, C. M. 1977. Some aspects of the epidemiology of tinea. Mycopathologia. 62:3-13.

    1724. Ravine, D., K. J. Turner, and M. P. Alpers. 1980. Genetic inheritance of susceptibility to tinea imbricata. J Med Genet. 17:342-8.

    1774. Rist, T. E., D. C. Abele, and J. M. Caves. 1974. Tinea faciale: an often misdiagnosed clinical entity. South Med J. 67:331-4.

    1794. Roldan, Y. B., S. Mata-Essayag, and C. Hartung. 2000. Erysipelas and tinea pedis. Mycoses. 43:181-3.

    1915. Serjeantson, S., and G. Lawrence. 1977. Autosomal recessive inheritance of susceptibility to tinea imbricata. Lancet. 1:13-5.

    Information here taken from doctorfungus.org

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