CASE #2: Tinea corporis

Tinea corporis, commonly known as ringworm, is a dermatophyte infection primarily found on the skin of the trunk and extremities. Since ancient times, dermatophytes have been infecting athletes, soldiers, and people from all walks of life. Dermatophytes are passed on via human-to-human, animal-to-human, soil-to-human, or soil-to-animal transmission.7 The most common dermatophytes causing tinea corporis include Trichophyton rubrum, Microsporum canis, and T. mentagrophytes.1,2

These pathogens have developed numerous mechanisms that allow them to adhere to the skin. Once there, the pathogens produce keratinases that break down keratin and allow for invasion of the fungi into keratinized tissues. Several host factors also affect the severity of the infection. Sebum has an inhibitory effect on dermatophytes, and if the host has few and inactive sebaceous glands, the infection could become severe. Infection also is increased if the host has many breaks in the skin, thus encouraging invasion of the pathogens. Pathogens that have infiltrated the skin usually remain limited to the keratinized tissue and do not invade deeper. They prefer the cooler temperature of the skin, and there are factors in the serum and host immune system that inhibit dermatophyte growth.

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Tinea corporis is a dermatophyte infection that is generally located in the stratum corneum and normally found on the skin of the trunk and extremities, excluding the scalp (tinea capitis), bearded areas (tinea barbae), nails (onychomycosis), hands (tinea manuum), feet (tinea pedis), and groin (tinea cruris). Worldwide, the most common pathogen is T. rubrum, followed by T. mentagrophytes.1 Although tinea corporis occurs most commonly in humid regions,2 there have been cases reported in all types of climates. Individuals with exposure to domestic animals (particularly kittens and puppies), occupational or recreational exposure (gymnasiums, locker rooms, wrestling, outdoor occupations), and immunosuppression have an increased rate of infection.1,8 This is primarily due to the increased chance of successful transmission of the pathogens responsible for tinea corporis. Areas on the body with increased hair follicles will have higher inflammatory responses because hair follicles serve as reservoirs for infection.1 Inflammation also depends on the type of dermatophyte that infected the host as well as the strength of the host’s immune response.

The incubation period is one to three weeks, and infection tends to spread centrifugally from the point of skin invasion.1 Because of the centrifugal spread, lesions often present as asymmetric, erythematous annular plaques with central clearing. When multiple lesions are present, they may coalesce to form polycyclic configurations. Papules, pustules, or vesicles may be found within the border of active lesions. Scaling is a predominant finding in tinea, although if treated with topical corticosteroids, this may be diminished. Lesions are often associated with pruritus and/or a burning sensation.

Three clinical variants of tinea corporis are Majocchi’s granuloma, tinea profunda, and tinea imbricata.1 A perifollicular granulomatous disorder, Majocchi’s is seen most commonly on the legs of women who have concomitant tinea pedis or onychomycosis (shaving the legs causes infected hairs to penetrate the wall of the follicle). Majocchi’s lesions present as erythematous patches or plaques that are studded with papules or papulonodules. Tinea profunda is caused by an excessive inflammatory response to a dermatophyte. T. concentricum is the cause of tinea imbricata, which is seen primarily along an equatorial band encompassing the South Pacific, Asia, and Central and South America.1,8 Lesions initially present as concentric annular rings of scaling that form extensive patches. With time, the lesions may spread and cover almost the entire skin surface. At this time, the concentric rings are seen as parallel lines of scales overlapping each other, resembling shingles on a roof (imbrex is another word for shingle).8

The sandwich sign is often present in tinea corporis and is distinguished by orthokeratosis or parakeratosis alternating in layers with basket-weave stratum corneum.4,5 Hyphae can often be seen in this area. Neutrophils are present in the stratum corneum, and spongiosis or intraepidermal vesicles form. Variable degrees of an inflammatory response may be seen.

Tinea corporis has many features that resemble other dermatologic conditions. Thus clinical observation, although very important, is insufficient for diagnosis. Proper specimen collection and laboratory testing is necessary to confirm the diagnosis. Most dermatophytes are able to grow on media containing cycloheximide;1 however, some important nondermatophyte fungi do not. A KOH test will determine if dermatophytes are present but will not differentiate between species. GA is a common misdiagnosis of tinea corporis, since there are many similar clinical features present in these erythematous annular lesions. As mentioned earlier, the use of topical corticosteroids may further mask the diagnosis by altering the presenting features. Other condtions commonly mistaken for tinea corporis include dermatitis, pityriasis versicolor, pityriasis rosea, parapsoriasis, impetigo, subacute lupus erythematosus, annular psoriasis, and erythema annulare centrifugum.

First-line therapy includes topical antifungals, as these are beneficial in treating localized dermatophyte infections and feature a quite limited side-effect profile. Treatment should be continued for at least one week after clinical resolution of the infection.3 The major side effect is a localized irritant or allergic contact dermatitis caused mainly by the vehicle through which the medication is delivered. Some advocate the use of a low-potency topical steroid to be used in combination with a topical antifungal to reduce inflammation. Oral antifungals are often required to treat certain dermatophyte infections, including those cases of tinea corporis that are resistant to topical treatment as well as tinea manuum, capitis and unguium.7

This patient was treated with clotrimazole (Desenex) cream, and the lesions resolved completely.

Dr. Robbins is a resident in the department of dermatology at Baylor College of Medicine in Houston. The author has no relationships to disclose relating to the content of this article.


1. JL Bolognia, JL Jorizzo, RP Rapini, eds. Dermatology, 2nd ed., St. Louis, Mo.: Mosby-Elsevier; 2008:1138-1140, 1145-1146, 1426-1429.

2. Fitzpatrick TB, Johnson RA, Wolff K, Suurmond R, eds. Color Atlas and Synopsis of Clinical Dermatology, 5th ed. New York, N.Y.: McGraw-Hill; 2005:128-129, 700-703.

3. TP Habif. Skin Disease: Diagnosis and Treatment. 2nd ed., Philadelphia, Pa.: Elsevier Mosby; 2005:250-253, 566-569.

4. RP Rapini. Practical Dermatopathology. Philadelphia, Pa.: Elsevier Mosby; 2005:99-100, 177.

5. DE Elder, R Elenitsas, BL Johnson, GF Murphy, X Xu, eds. Lever’s Histopathology of the Skin. 10th ed., Philadelphia, Pa.: Lippincott Williams & Wilkins; 2009:361-364, 593-594.

6. Marcus DV, Mahmoud BH, Hamzavi IH. Granuloma annulare treated with rifampin, ofloxacin, and minocycline combination therapy. Arch Dermatol. 2009;145:787-789.

7. Andrews MD, Burns M. Common tinea infections in children. Am Fam Physician. 2008;77:1415-1420. 

8. Paller AS, Mancini AJ Hurwitz Clinical Pediatric Dermatology. 3rd ed. Philadelphia, Pa.: Elsevier Saunders; 2006.456-458.

All electronic documents accessed February 15, 2011.