Tinea Corporis

Back

Practice Essentials

Tinea corporis is a superficial dermatophyte infection characterized by either inflammatory or noninflammatory lesions on the glabrous skin (ie, skin regions other than the scalp, groin, palms, and soles).[1] Three anamorphic (asexual or imperfect) genera cause dermatophytoses: Trichophyton, Microsporum, and Epidermophyton. Dermatophytes may infect humans (anthropophilic) or nonhuman mammals (zoophilic), or they may reside primarily in the soil (geophilic).[2, 3]

Signs and symptoms

The lesion typically begins as an erythematous, scaly plaque that may rapidly worsen (see the image below). These scaly plaques typically have a raised border with peripheral scale. This scale is usually trailing scale, with the free edge of the scale pointed inward.



View Image

Large, erythematous, scaly plaque.

Following central resolution, the lesion may become annular in shape (see the image below).



View Image

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 that typically develop 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[4, 5] ; 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 Trichophyton concentricum[6] and is recognized clinically by its distinct, scaly plaques arranged in concentric rings.

Tinea incognito

This variant is tinea corporis with an altered, nonclassic presentation resulting from corticosteroid treatment.[7]

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. See Workup for more details. 

A fungal culture, which is often used as an adjunct to KOH for diagnosis, is more specific than KOH for detecting a dermatophyte infection. Accordingly, if clinical suspicion is high but the KOH result is negative, a fungal culture should be obtained. A fungal culture is typically performed on a dermatophyte test medium (DTM). A DTM contains chloramphenicol, gentamicin, and cycloheximide to inhibit bacteria and some saprophytic fungal growth.

If KOH and fungal culture clinical evaluations are inconclusive, a polymerase chain reaction (PCR) assay for fungal DNA identification may be ordered.[8]

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

Histology

A skin biopsy specimen with hematoxylin and eosin (H&E) 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 H&E 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 sterol in the fungal cell membrane.

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.[9]

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. Resistance to oral agents is also prevalent in some areas, though not all treatment failures are related to resistance.[10, 11, 12]

See Treatment and Medication for more detail.

Pathophysiology

Dermatophytes preferentially inhabit the nonliving, cornified layers of the skin, hair, and nail, which are attractive for the warm, moist environment conducive to fungal proliferation. Fungi may release keratinases and other enzymes to invade deeper into the stratum corneum, though 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.

After 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 shedding the infected skin and leaving new, healthy skin central to the advancing lesion. Elimination of dermatophytes is achieved by cell-mediated immunity.

T 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.[13]

Etiology

Tinea corporis can be caused by a variety of dermatophytes, though prevalence and patient history are very helpful in identifying the most likely organism. Internationally, the most commonly reported cause has been T rubrum.Trichophyton tonsurans, Trichophyton mentagrophytes,[7, 14] Trichophyton interdigitale, Trichophyton verrucosum,[15] Microsporum canis,Microsporum gypseum,[6]  and Microsporum langeronii[16] are also known to produce infection. Tinea imbricata is caused by T concentricum.

The organism Trichophyton indotineae (previously classified as type VIII T mentagrophytes) is a pathogen of growing concern as a cause of tinea corporis and cruris.[17]  It is often resistant to commonly used agents (eg, terbinafine).

Dermatophytoses may be acquired from different sources (eg, 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, in hair brushes or 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.[14] Infection with M gypseum, a geophilic organism, can mimic tinea imbricata in presentation.

Because fungal arthroconidia can survive in the environment, outbreaks may recur.

Epidemiology

United States and international statistics

Dermatophyte infections are the most common fungal infections in the United States and among the most common sources of skin disease worldwide. Over the period from 2005 to 2014, these infections accounted for 4,981,444 outpatient visits in the United States, and in 2019, the direct medical cost of managing them was approximately $845 million.[18]

Tinea corporis is a common infection more often seen in typically hot, humid climates. Previous studies cited T rubrum as the source of nearly 50% of tinea corporis cases in the United States.[19]  In a 2024 study using data from a major US commercial laboratory (Labcorp), Zarzeka et al reported 15,563 cases of tinea corporis for the period from March 1, 2019, to March 1, 2023[20] ; the most common causative organism was T tonsurans, followed by T rubrum and then by yeasts (with Candida species accounting for the majority), nondermatophyte molds, and unspecified fungus.

T tonsurans is the dermatophyte that most commonly causes tinea capitis, and people with an anthropophilic tinea capitis infection are more likely to develop associated tinea corporis. Consequently, the prevalence of tinea corporis caused by T tonsurans has been increasing.[21, 20]

M canis has been associated with 14% of tinea corporis infections. Seyfarth et al reported a rare case of Microsporum fulvum skin infection (forearm), identified by ITS sequencing and mass spectrometry.[22]

A 5-year study (N = 2370) from Kuwait reported that fungal skin infections remained prevalent in that country, specifically in the capital area.[23] In patients with dermatophytes, six species were isolated: T mentagrophytes (39%), M canis (16%), T rubrum (10%), Epidermophyton floccosum (6.2%), Trichophyton violaceum (2.4%), and T verrucosum (0.4%).[23]  There is evidence to suggest that the T mentagrophytes variant T interdigitale can be found on all body sites, not just the feet.[24]

Age- and sex-related demographics

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.

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.

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

History

Symptoms, contact history, recent travel, and international residence are relevant clues in the history.

Patients with tinea corporis may have variable symptoms; they may also 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 T concentricum.[6]

Tinea incognito is tinea corporis with an altered, nonclassic presentation resulting from corticosteroid treatment.[7] This is a variant that is often difficult to diagnose in that patients often report a chronic rash. A clue to tinea incognito is that the patient may report a rash that has gotten worse after applying topical steroids.

Physical Examination

Tinea corporis can manifest in a variety of ways. Typically, the lesion begins as an erythematous, scaly plaque that may rapidly worsen and enlarge (see the image below).



View Image

Large, erythematous, scaly plaque.

Following central resolution, the lesion may become annular in shape (see the image below).[25]



View Image

Annular plaque.

As a result of the inflammation, scale, crust, papules, vesicles, and even bullae can develop, especially in the advancing border.[26]

Rarely, tinea corporis can present as purpuric macules, called tinea corporis purpurica.[27] One report described two cases of tinea corporis purpurica resulting from self-inoculation with T violaceum.[28]

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 that typically occur 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.

Laboratory Studies

A potassium hydroxide (KOH) examination of skin scrapings may be diagnostic in tinea corporis. A KOH test is a microscopic preparation used to visualize fungal elements removed from the skin's stratum corneum. It is performed as follows:

A fungal culture is often used as an adjunct to KOH for diagnostic purposes. Fungal culture is more specific than KOH for detecting a dermatophyte infection; accordingly, if clinical suspicion is high but KOH testing yields a negative result, a fungal culture is indicated.

A few culture mediums are available for dermatophyte growth. Sabouraud agar, which contains neopeptone or polypeptone agar and glucose, is often used; 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 contains antibiotics. Frequently, dermatophyte test medium (DTM) is used. It contains antibacterial (ie, gentamicin, chloramphenicol) 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 (PCR) for fungal DNA identification can be applied.[8]

For atypical presentations of tinea corporis, further evaluation for HIV infection, another immunocompromised state, or both should be considered.

Histologic Findings

A skin biopsy specimen with hematoxylin and eosin (H&E) 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 H&E stain, but special fungal stains (eg, periodic acid-Schiff, Gomori methenamine silver) may be required. Hyphae typically are present at different levels of the stratum corneum and usually are parallel to the epidermis.

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.[29] Topical azoles and allylamines show high rates of clinical efficacy. These agents inhibit the synthesis of ergosterol, a major fungal cell membrane sterol.[30]

Topical azoles (eg, econazole, ketoconazole, clotrimazole, miconazole, oxiconazole, sulconazole, sertaconazole) inhibit the enzyme lanosterol 14-alpha-demethylase, a cytochrome P-450 (CYP-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 a newer topical azole that has been found to compare favorably with other agents.[31] It has fungistatic and anti-inflammatory abilities and is used as a broad-spectrum agent. Some data suggest that sertaconazole is as effective as fungicidal agents.[32] It may have a reservoir effect and therefore is a good choice for noncompliant patients. In-vitro data indicate that it has anti-itch properties.[33]

Luliconazole is an imidazole topical cream approved by the FDA for treatment of interdigital tinea pedis, tinea cruris, and tinea corporis. The safety and efficacy of luliconazole topical cream 1%  for tinea corporis vs vehicle cream was evaluated in a randomized, double-blind, vehicle-controlled, multicenter clinical trial that included 75 patients aged 2-17 years with a clinical- and culture-confirmed diagnosis.[34] About 2.5 cm of topical cream was applied of the surrounding skin once daily for 7 days. Complete clearance was observed in 71% of patients in the luliconazole group compared with 36% in the vehicle cream group.

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]  T indotineae has exhibited significant resistance to terbinafine[17] ; oral itraconazole is preferred treatment for infections caused by this organism.[35, 36]

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 it should be applied only for the first few days of treatment. Prolonged use of steroids can lead to persistent and recurrent infections, longer duration of treatment regimens, and various adverse effects (eg, skin atrophy, striae, and telangiectasias).

Systemic therapy may be indicated for cases of tinea corporis that involve extensive skin infection, immunosuppression, resistance to topical antifungal therapy, or comorbidities of tinea capitis or tinea unguium. Use of oral agents requires attention to potential drug interactions and monitoring for adverse effects. Resistance to oral agents is also prevalent in some areas, though not all treatment failures are related to resistance.[10, 11, 12]

The mechanism through which oral micronized griseofulvin acts against dermatophytes is disruption of the microtubule mitotic spindle formation in metaphase, which causes arrest of fungal cell mitosis. A dosage of 10 mg/kg/day for 4 weeks is effective. In addition, griseofulvin induces the CYP-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. Minimal inhibitory concentrations (MICs) for common dermatophytes tend to be higher for griseofulvin than for other agents, and response rates may be lower, especially at labeled doses.[37]

Systemic azoles (eg, fluconazole, itraconazole, ketoconazole) function similarly to the topical agents, causing cell membrane destruction.[9]

Oral ketoconazole at 3-4 mg/kg/day may be given. However, this agent carries an associated risk of hepatitis (< 1 in 10,000 cases) and is rarely used orally for dermatophyte infections.

Fluconazole at 50-100 mg/day or 150 mg once weekly for 2-4 weeks is used with good results.

Oral itraconazole at 100 mg/day for 2 weeks shows high efficacy. At a dosage of 200 mg/day, the treatment duration can be reduced to 1 week. However, the CYP-450 activity of itraconazole allows potential interactions with other commonly prescribed drugs.[38] When it is appropriate to prescribe itraconazole, there may be some advantage to giving it with whole milk so as to increase absorption.[39]

In a study that used the E-test to assess the antifungal susceptibility of T rubrum, voriconazole was found to be the most active of the azole drugs, with fluconazole the least active.[40]

Oral terbinafine may be used at a dosage of 250 mg/day for 2 weeks; however, the potential exists for CYP-450 (specifically, CYP-2D6) drug interactions with this agent.

Systemic therapy is needed when the infection involves hair follicles (eg, Majocchi granuloma). In this case, topical therapy may serve as adjunct treatment with the oral medication.

For severe cases of tinea incognito, oral antifungal treatment may be necessary. Ii is important to note is that if a dermatophyte infection is suspected, a topical steroid should not be prescribed. Often, patients are coprescribed corticosteroids to provide an anti-inflammatory effect and antifungal cream to hasten the resolution of the rash. In true dermatophyte infections, however, such coprescription leads to severe worsening of the skin lesions. Antifungal cream should be tried first for least 14 days. If there is no improvement, other dermatoses can then be considered.

The preferred treatment for tinea imbricata is griseofulvin or terbinafine, though some resistance has developed to oral griseofulvin.[41]  A study (N = 20) from the Philippines cited significant decreases in pruritus and disease severity with the use of a botanical extract.[42]

Surgical Care

Surgical treatment usually is not indicated, except for drainage of superficial vesicles, bullae, pustules, or deep abscesses.

Complications

Tinea corporis may recur if therapy does not result in complete eradication of the organism, as may occur if patients stop applying topical therapy too soon or if the organism is resistant to the antifungal agent used. Reinfection may develop if a reservoir (eg, 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.

Id reaction

Dermatitis caused by exogenous agents initially arises at the site of contact. Not infrequently, additional patches of eczema develop at distant sites. This phenomenon, termed secondary dissemination, can occur with severe tinea pedis. Disseminated eczema appears a few days to weeks later than the primary lesions, tends to follow a strikingly symmetric distribution pattern, and shows a predilection for analogous body sites (eg, extensor aspects of the lower and upper extremities, palms, and soles). It may even arise in the absence of and without a preceding “primary” eczema (eg, in nummular dermatitis).

Prevention

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

Long-Term Monitoring

Follow-up care for tinea corporis should be determined on the basis of patient need, severity of infection, and response to treatment. The rate of relapse is high.[43]

Medication Summary

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.

It is important to remember that dermatophytosis of the scalp, nails, and hair follicles (Majocchi granuloma) requires treatment with oral antifungals to eradicate fungal infection. Tinea corporis, tinea pedis, and tinea cruris are typically treated with topical antifungals such as ketoconazole cream, with good response.

For patients with chronic tinea pedis or tinea cruris and large body habitus or a tendency for hyperhidrosis, a miconazole powder formulation as a preventive measure may be beneficial. This is after the active lesions have been treated with a topical cream.

What is tinea corporis (ringworm)?What are the signs and symptoms of tinea corporis (ringworm)?How do tinea corporis (ringworm) infections due to zoophilic and geophilic dermatophytes differ from those caused by anthropophilic microbes?How are presentations of tinea corporis (ringworm) in immunocompromised patients often characterized?What is Majocchi granuloma, and how is this variant of tinea corporis (ringworm) characterized?What is the presentation of tinea corporis (ringworm) gladiatorum?What is the presentation of tinea imbricata?What is tinea incognito?How is a potassium hydroxide (KOH) exam used in the diagnosis of tinea corporis (ringworm)?When is a fungal culture used in the diagnosis of tinea corporis (ringworm)?When is a PCR assay used in the diagnosis of tinea corporis (ringworm)?Which conditions should be considered when the presentation of tinea corporis (ringworm) is atypical?How are the histologic findings of tinea corporis (ringworm) characterized?What is the treatment of choice for localized tinea corporis (ringworm) infection?What is the role of allylamines in the treatment of tinea corporis (ringworm)?When is systemic therapy indicated in the treatment of tinea corporis (ringworm)?What is tinea corporis (ringworm)?What is the pathophysiology of tinea corporis (ringworm)?How is Trichophyton rubrum characterized in tinea corporis (ringworm)?Which dermatophytes most commonly cause tinea corporis (ringworm)?What are common sources of dermatophytes that cause tinea corporis (ringworm)?In which climates is tinea corporis (ringworm) most common?What are the sex-related demographics for tinea corporis (ringworm)?What are the age-related demographics for tinea corporis (ringworm)?What is the prognosis of localized tinea corporis (ringworm)?What patient education resources are available for tinea corporis (ringworm)?What information should be collected in the history of a patient presenting with tinea corporis (ringworm)?What is the range of symptoms of tinea corporis (ringworm)?How does someone contract tinea corporis (ringworm)?What is the presentation of Majocchi granuloma tinea corporis (ringworm)?What is tinea corporis (ringworm) gladiatorum?What is tinea imbricata?What is tinea incognito?What are the signs and symptoms of tinea corporis (ringworm)?What are the potential complications of inflammation due to tinea corporis (ringworm)?What is tinea corporis (ringworm) purpurica?How do tinea corporis (ringworm) infections due to zoophilic and geophilic dermatophytes differ from those caused by anthropophilic microbes?Which conditions should be considered when the presentation of tinea corporis (ringworm) is atypical?What are the characteristics of Majocchi granuloma tinea corporis (ringworm)?What are the characteristics of tinea corporis (ringworm) gladiatorum?What are the clinical characteristics of tinea imbricata?What are the differential diagnoses for Tinea Corporis?What lab study is usually used to diagnose tinea corporis (ringworm)?When is a fungal culture indicated in the workup of tinea corporis (ringworm)?Which media are often used for fungal culture in lab studies for tinea corporis (ringworm)?How can the culture medium affect the results in a fungal culture for tinea corporis (ringworm)?When is a PCR assay used in the workup of tinea corporis (ringworm)?Which tests should be considered in an atypical presentation of tinea corporis (ringworm)?What are the histologic findings of tinea corporis (ringworm)?When is topical therapy recommended for the management of tinea corporis (ringworm), and how effective is it?What is the mechanism of action of topical azoles in the treatment of tinea corporis (ringworm)?What is luliconazole (Luzu), and what is its role in the treatment of tinea infections (ringworm)?What is the efficacy of luliconazole (Luzu) in the treatment of tinea corporis?What is the mechanism of action of allylamines in the treatment of tinea corporis (ringworm)?What is the mechanism of action of ciclopirox olamine in the treatment of tinea corporis (ringworm)?What is the role of topical corticosteroids in the treatment of tinea corporis (ringworm)?When is systemic therapy indicated in the treatment of tinea corporis (ringworm)?How is an oral micronized griseofulvin used in the treatment of tinea corporis (ringworm)?How are systemic azoles used in the treatment of tinea corporis (ringworm)?What is the role of oral ketoconazole in the treatment of tinea corporis (ringworm)?What is the recommended dosage of fluconazole in the treatment of tinea corporis (ringworm)?What is the recommended dosage of oral itraconazole in the treatment for tinea corporis (ringworm)?Which of the azole drugs is most and least active in the treatment of tinea corporis (ringworm)?What is the recommended dosage of oral terbinafine in the treatment of tinea corporis (ringworm)?When is systemic therapy indicated in the treatment of tinea corporis (ringworm)?What is the preferred treatment for tinea imbricata?When is surgical treatment indicated in the treatment of tinea corporis (ringworm)?What complications can arise in tinea corporis (ringworm)?How is the spread of tinea corporis infection (ringworm) prevented?What is the recommended follow-up care for tinea corporis (ringworm)?What are the goals of pharmacotherapy for the treatment of tinea corporis (ringworm)?Which medications in the drug class Topical allylamines are used in the treatment of Tinea Corporis?Which medications in the drug class Topical pyridones are used in the treatment of Tinea Corporis?Which medications in the drug class Topical benzylamines are used in the treatment of Tinea Corporis?Which medications in the drug class Systemic azoles are used in the treatment of Tinea Corporis?Which medications in the drug class Systemic allylamines are used in the treatment of Tinea Corporis?Which medications in the drug class Other systemic antifungals are used in the treatment of Tinea Corporis?Which medications in the drug class Topical azoles are used in the treatment of Tinea Corporis?

Author

Shweta Shukla, MD, Resident Physician, Department of Dermatology, State University of New York Downstate Medical Center

Disclosure: Nothing to disclose.

Coauthor(s)

Amor Khachemoune, MD, Director of Mohs and Laser Surgery, Dermatopathology, Premier Dermatology, PC; Associate Program Director, Mohs Micrographic Surgery Fellowship Training Program, Co-Chief of Dermatologic Surgery, Consulting Staff Physician, Dermatology Service, VA Hospital of Brooklyn; Mohs Surgeon, Veterans Affairs Hospital of Baltimore; Chair Professor, Vitiligo Research Chair, Department of Dermatology, King Saud University; Consultant Dermatologist, Kadina Medical Center, KSA

Disclosure: Nothing to disclose.

Specialty Editors

Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Disclosure: Nothing to disclose.

Rosalie Elenitsas, MD, Herman Beerman Professor of Dermatology, University of Pennsylvania School of Medicine; Director, Penn Cutaneous Pathology Services, Department of Dermatology, University of Pennsylvania Health System

Disclosure: Received royalty from Lippincott Williams Wilkins for textbook editor.

Chief Editor

Dirk M Elston, MD, Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Jack L Lesher, Jr, MD, Chief, Professor, Department of Internal Medicine, Section of Dermatology, Medical College of Georgia

Disclosure: Nothing to disclose.

Janet Fairley, MD, Professor and Head, Department of Dermatology, University of Iowa, Roy J and Lucille A Carver College of Medicine

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors Mary Elizabeth Rushing Lott, MD and Gwendolyn Zember, MD, to the development and writing of this article.

References

  1. Pires CA, Cruz NF, Lobato AM, Sousa PO, Carneiro FR, Mendes AM. Clinical, epidemiological, and therapeutic profile of dermatophytosis. An Bras Dermatol. 2014 Mar-Apr. 89 (2):259-64. [View Abstract]
  2. Jain S, Kabi S, Swain B. Current Trends of Dermatophytosis in Eastern Odisha. J Lab Physicians. 2020 Mar. 12 (1):10-14. [View Abstract]
  3. Leung AK, Lam JM, Leong KF, Hon KL. Tinea corporis: an updated review. Drugs Context. 2020. 9:[View Abstract]
  4. Adams BB. Tinea corporis gladiatorum. J Am Acad Dermatol. 2002 Aug. 47 (2):286-90. [View Abstract]
  5. Ilkit M, Ali Saracli M, Kurdak H, Turac-Bicer A, Yuksel T, Karakas M, et al. Clonal outbreak of Trichophyton tonsurans tinea capitis gladiatorum among wrestlers in Adana, Turkey. Med Mycol. 2010 May. 48 (3):480-5. [View Abstract]
  6. Sun PL, Ho HT. Concentric rings: an unusual presentation of tinea corporis caused by Microsporum gypseum. Mycoses. 2006 Mar. 49 (2):150-1. [View Abstract]
  7. Sánchez-Castellanos ME, Mayorga-Rodríguez JA, Sandoval-Tress C, Hernández-Torres M. Tinea incognito due to Trichophyton mentagrophytes. Mycoses. 2007 Jan. 50 (1):85-7. [View Abstract]
  8. 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. [View Abstract]
  9. Leyden J. Pharmacokinetics and pharmacology of terbinafine and itraconazole. J Am Acad Dermatol. 1998 May. 38 (5 Pt 3):S42-7. [View Abstract]
  10. Singh S, Shukla P. End of the road for terbinafine? Results of a pragmatic prospective cohort study of 500 patients. Indian J Dermatol Venereol Leprol. 2018 Sep-Oct. 84 (5):554-557. [View Abstract]
  11. Singh A, Masih A, Khurana A, Singh PK, Gupta M, Hagen F, et al. High terbinafine resistance in Trichophyton interdigitale isolates in Delhi, India harbouring mutations in the squalene epoxidase gene. Mycoses. 2018 Jul. 61 (7):477-484. [View Abstract]
  12. Sardana K, Kaur R, Arora P, Goyal R, Ghunawat S. Is Antifungal Resistance a Cause for Treatment Failure in Dermatophytosis: A Study Focused on Tinea Corporis and Cruris from a Tertiary Centre?. Indian Dermatol Online J. 2018 Mar-Apr. 9 (2):90-95. [View Abstract]
  13. Mapelli ET, Borghi E, Cerri A, Sciota R, Morace G, Menni S. Tinea corporis due to Trichophyton rubrum in a woman and Tinea capitis in her 15-day-old baby: molecular evidence of vertical transmission. Mycopathologia. 2012 Mar. 173 (2-3):135-8. [View Abstract]
  14. 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. 2006 Jul. 55 (1):153-4. [View Abstract]
  15. Placzek M, van den Heuvel ME, Flaig MJ, Korting HC. Perniosis-like tinea corporis caused by Trichophyton verrucosum in cold-exposed individuals. Mycoses. 2006 Nov. 49 (6):476-9. [View Abstract]
  16. Carod JF, Ratsitorahina M, Raherimandimby H, Hincky Vitrat V, Ravaolimalala Andrianaja V, Contet-Audonneau N. Outbreak of Tinea capitis and corporis in a primary school in Antananarivo, Madagascar. J Infect Dev Ctries. 2011 Oct 13. 5 (10):732-6. [View Abstract]
  17. Avery EG, Ricciuto DR, Kus JV. Refractory tinea corporis or cruris caused by Trichophyton indotineae. CMAJ. 2024 Aug 11. 196 (27):E940. [View Abstract]
  18. Kruithoff C, Gamal A, McCormick TS, Ghannoum MA. Dermatophyte Infections Worldwide: Increase in Incidence and Associated Antifungal Resistance. Life (Basel). 2023 Dec 19. 14 (1):[View Abstract]
  19. Foster KW, Ghannoum MA, Elewski BE. Epidemiologic surveillance of cutaneous fungal infection in the United States from 1999 to 2002. J Am Acad Dermatol. 2004 May. 50 (5):748-52. [View Abstract]
  20. Zarzeka D, Benedict K, McCloskey M, Lockhart SR, Lipner SR, Gold JAW. Current epidemiology of tinea corporis and tinea cruris causative species: Analysis of data from a major commercial laboratory, United States. J Am Acad Dermatol. 2024 Sep. 91 (3):559-562. [View Abstract]
  21. Hryncewicz-Gwóźdź A, Beck-Jendroschek V, Brasch J, Kalinowska K, Jagielski T. Tinea capitis and tinea corporis with a severe inflammatory response due to Trichophyton tonsurans. Acta Derm Venereol. 2011 Oct. 91 (6):708-10. [View Abstract]
  22. Seyfarth F, Goetze S, Erhard M, Burmester A, Elsner P, Hipler UC. [Infection with a rare geophilic dermatophyte]. Hautarzt. 2010 Aug. 61 (8):694-9. [View Abstract]
  23. 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. 2010 Apr. 169 (4):241-6. [View Abstract]
  24. Dhib I, Khammari I, Yaacoub A, Hadj Slama F, Ben Saïd M, Zemni R, et al. Relationship Between Phenotypic and Genotypic Characteristics of Trichophyton mentagrophytes Strains Isolated from Patients with Dermatophytosis. Mycopathologia. 2017 Jun. 182 (5-6):487-493. [View Abstract]
  25. Diep D, Calame A, Cohen PR. Tinea Corporis Masquerading as a Diffuse Gyrate Erythema: Case Report and a Review of Annular Lesions Mimicking a Dermatophyte Skin Infection. Cureus. 2020 Jun 30. 12 (6):e8935. [View Abstract]
  26. Ziemer M, Seyfarth F, Elsner P, Hipler UC. Atypical manifestations of tinea corporis. Mycoses. 2007. 50 Suppl 2:31-5. [View Abstract]
  27. Kim HS, Cho BK, Oh ST. A case of tinea corporis purpurica. Mycoses. 2007 Jul. 50 (4):314-6. [View Abstract]
  28. Romano C, Massai L, Strangi R, Feci L, Miracco C, Fimiani M. Tinea corporis purpurica and onychomycosis caused by Trichophyton violaceum. Mycoses. 2011 Mar. 54 (2):175-8. [View Abstract]
  29. Weinstein A, Berman B. Topical treatment of common superficial tinea infections. Am Fam Physician. 2002 May 15. 65 (10):2095-102. [View Abstract]
  30. Tsunemi Y. Oral Antifungal Drugs in the Treatment of Dermatomycosis. Med Mycol J. 2016. 57 (2):J71-5. [View Abstract]
  31. Chatterjee D, Ghosh SK, Sen S, Sarkar S, Hazra A, De R. Efficacy and tolerability of topical sertaconazole versus topical terbinafine in localized dermatophytosis: A randomized, observer-blind, parallel group study. Indian J Pharmacol. 2016 Nov-Dec. 48 (6):659-664. [View Abstract]
  32. Choudhary S, Bisati S, Singh A, Koley S. Efficacy and Safety of Terbinafine Hydrochloride 1% Cream vs. Sertaconazole Nitrate 2% Cream in Tinea Corporis and Tinea Cruris: A Comparative Therapeutic Trial. Indian J Dermatol. 2013 Nov. 58 (6):457-60. [View Abstract]
  33. Liebel F, Lyte P, Garay M, Babad J, Southall MD. Anti-inflammatory and anti-itch activity of sertaconazole nitrate. Arch Dermatol Res. 2006 Sep. 298 (4):191-9. [View Abstract]
  34. Luzu (luliconazole topical cream 1%) [package insert]. Bridgewater, NJ: Bausch health Companies. April 2020. Available at
  35. Nenoff P, Klonowski E, Uhrlaß S, Schaller M, Paasch U, Mayser P. [Dermatomycoses: topical and systemic antifungal treatment]. Dermatologie (Heidelb). 2024 Aug. 75 (8):655-673. [View Abstract]
  36. Khurana A, Agarwal A, Agrawal D, Panesar S, Ghadlinge M, Sardana K, et al. Effect of Different Itraconazole Dosing Regimens on Cure Rates, Treatment Duration, Safety, and Relapse Rates in Adult Patients With Tinea Corporis/Cruris: A Randomized Clinical Trial. JAMA Dermatol. 2022 Sep 14. 158 (11):1269-78. [View Abstract]
  37. Mahajan S, Tilak R, Kaushal SK, Mishra RN, Pandey SS. Clinico-mycological study of dermatophytic infections and their sensitivity to antifungal drugs in a tertiary care center. Indian J Dermatol Venereol Leprol. 2017 Jul-Aug. 83 (4):436-440. [View Abstract]
  38. Schreuder MF, van de Kar NC, Brüggemann RJ. Drug-Drug Interactions in Treatment Using Azole Antifungal Agents. JAMA. 2016 Jun 21. 315 (23):2622. [View Abstract]
  39. Chen S, Ran Y, Dai Y, Lama J, Hu W, Zhang C. Administration of Oral Itraconazole Capsule with Whole Milk Shows Enhanced Efficacy As Supported by Scanning Electron Microscopy in a Child with Tinea Capitis Due to Microsporum canis. Pediatr Dermatol. 2015 Nov-Dec. 32 (6):e312-3. [View Abstract]
  40. da Silva Barros ME, de Assis Santos D, Soares Hamdan J. Antifungal susceptibility testing of Trichophyton rubrum by E-test. Arch Dermatol Res. 2007 May. 299 (2):107-9. [View Abstract]
  41. 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. 2004 Jan. 150 (1):119-26. [View Abstract]
  42. Eusebio-Alpapara KMV, Dofitas BL, Balita-Crisostomo CLA, Tioleco-Ver GMS, Jandoc LE, Frez MLF. Senna (Cassia) alata (Linn.) Roxb. leaf decoction as a treatment for tinea imbricata in an indigenous tribe in Southern Philippines. Mycoses. 2020 Nov. 63 (11):1226-1234. [View Abstract]
  43. Majid I, Sheikh G, Kanth F, Hakak R. Relapse after Oral Terbinafine Therapy in Dermatophytosis: A Clinical and Mycological Study. Indian J Dermatol. 2016 Sep-Oct. 61 (5):529-33. [View Abstract]

Large, erythematous, scaly plaque.

Annular plaque.

Large, erythematous, scaly plaque.

Annular plaque.

Annular plaque.

Large, erythematous, scaly plaque.

Tinea corporis. Courtesy of Wikimedia Commons (https://commons.wikimedia.org/wiki/File:Tinea_corporis.png).

Dermatophytosis or ringworm with mildly raised boarder and central clearing. Courtesy of Wikimedia Commons [James Heilman, MD] (https://commons.wikimedia.org/wiki/File:Yeartinfection.JPG).