Signs and symptoms of Tinea Corporis NYC New York, NY

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;[3, 4] 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[5] 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.[6]

See Clinical Presentation for more detail.

Diagnosis
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.[7]

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

Histology

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.

Management
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.[8]

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