Tinea Corporis 

Updated: Jul 09, 2018
Author: Jack L Lesher, Jr, MD; Chief Editor: Dirk M Elston, MD 

Overview

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).

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[2, 3] ; 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[4] 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.[5]

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.[6]

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 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.[7]

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, although not all treatment failures are related to resistance.[8, 9, 10]

See Treatment and Medication for more detail.

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.[11]

Etiology

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,[5, 12] Trichophyton interdigitale, Trichophyton verrucosum,[13] Microsporum canis, and Microsporum gypseum[4] 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.[12]  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.

Epidemiology

Frequency

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.[14, 15] 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.[16] 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 been reported, identified by ITS sequencing and mass spectrometry.[17]

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%).[18]  Evidence suggests that T mentagrophytes variant interdigitale can be found on all body sites, not just the feet.[19]

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.

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.

Patient Education

For patient education resources, see the Skin Conditions & Beauty Center. Also see the patient education article Ringworm on Body.

 

Presentation

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.[2, 3]

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.[4]

Tinea incognito is tinea corporis with an altered, nonclassic presentation due to corticosteroid treatment.[5]

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, as shown in the image below.

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.

As a result of the inflammation, scale, crust, papules, vesicles, and even bullae can develop, especially in the advancing border.[20]

Rarely, tinea corporis can present as purpuric macules, called tinea corporis purpurica.[21] One report describes 2 cases of tinea corporis purpurica resulting from self-inoculation with Trichophyton violaceum.[22]

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.

 

DDx

 

Workup

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. The sample should be taken from the active border of a lesion because this region provides the highest yield of fungal elements. A KOH preparation from a vesicular lesion should be made from the roof of the vesicle. The KOH helps dissolve the keratin and leaves fungal elements intact, revealing numerous septate, branching hyphae amongst epithelial cells. A counterstain, such as chlorazol black E or Parker blue-black ink, may help visualize hyphae under the microscope.

A fungal culture is often used as an adjunct to KOH for diagnosis. Fungal culture 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.

A few culture mediums are available for dermatophyte growth. Sabouraud agar containing neopeptone or polypeptone agar and glucose is often used for fungal culture. 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 has antibiotics. Commonly, dermatophyte test medium (DTM) is used. It contains antibacterial (ie, gentamicin, chlortetracycline) 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 for fungal DNA identification can be applied.[6]

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

Histologic Findings

A skin biopsy specimen with 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.

 

Treatment

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.[23] Topical azoles and allylamines show high rates of clinical efficacy. These agents inhibit the synthesis of ergosterol, a major fungal cell membrane sterol.[24]

The topical azoles (eg, econazole, ketoconazole, clotrimazole, miconazole, oxiconazole, sulconazole, sertaconazole) 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. The weakened dermatophyte is unable to reproduce and is slowly killed by fungistatic action. Sertaconazole nitrate is one of the newest topical azoles and compares favorably to other agents.[25]  It has fungistatic and anti-inflammatory abilities and is used as a broad-spectrum agent. Some data suggest it is as effective and fungicidal agents.[26]  It may have a reservoir effect and therefore is a good choice for noncompliant patients. Lastly, Liebel et al published in vitro data in 2006, reporting this drug has anti-itch properties.[27]

Luliconazole (Luzu) is an imidazole topical cream approved by the FDA in November 2013 for treatment of interdigital tinea pedis, tinea cruris, and tinea corporis. Approval was based on the results of three positive studies that evaluated 679 patients with either tinea pedis, corporis, or cruris.[28, 29]

The safety and efficacy of luliconazole topical cream 1% for tinea corporis was evaluated in a randomized, double-blind, vehicle-controlled, multicenter clinical trial in 75 individuals aged 2-17 years with a clinical- and culture-confirmed diagnosis of tinea corporis. Patients were randomized to receive luliconazole or vehicle cream. About 1-inch 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.[29]

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.[7]

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

Systemic therapy may be indicated for tinea corporis that includes extensive skin infection, immunosuppression, resistance to topical antifungal therapy, and 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, although not all treatment failures are related to resistance.[8, 9, 10]

The mechanism of action of oral micronized griseofulvin against dermatophytes is disruption of the microtubule mitotic spindle formation in metaphase, causing arrest of fungal cell mitosis. A dose of 10 mg/kg/d for 4 weeks is effective. In addition, griseofulvin induces the cytochrome P-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 for common dermatophytes tend to be higher for griseofulvin than for other agents, and response rates may be lower, especially at labeled doses.[30]

Systemic azoles (eg, fluconazole, itraconazole, ketoconazole) function similar to the topical agents, causing cell membrane destruction.[7]

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

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

Oral itraconazole in doses of 100 mg/d for 2 weeks shows high efficacy. With an increased dose of 200 mg/d, the treatment duration can be reduced to 1 week. However, the cytochrome P-450 activity of itraconazole allows for potential interactions with other commonly prescribed drugs.[31] When it is appropriate to prescribe the drug, there may be some advantage to giving itraconazole with whole milk to increase absorption.[32]

Based on E-test for susceptibility of T rubrum, voriconazole was the most active and fluconazole was the least active of the azole drugs.[33]

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

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

The preferred treatment for tinea imbricata is griseofulvin or terbinafine, although some resistance has developed to oral griseofulvin.[34]

Surgical Care

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

Complications

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

Prevention

Imperative for preventing the spread of a dermatophyte infection is to discourage close contact between infected and noninfected individuals and to stop the sharing of fomites (eg, 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 per patient need, severity of infection, and response to treatment. The rate of relapse is high.[35]

 

Medication

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.

Topical allylamines

Naftifine 1% cream or gel (Naftin)

Naftifine is a broad-spectrum antifungal agent that appears to interfere with sterol biosynthesis by inhibiting the enzyme squalene 2,3-epoxidase. This inhibition results in decreased amounts of sterols, causing cell death. If no clinical improvement occurs after 4 weeks, reevaluate patient.

Terbinafine topical (Lamisil)

Terbinafine topical has fungicidal activity; it is a synthetic allylamine derivative that inhibits squalene epoxidase, a key enzyme in sterol biosynthesis of fungi, resulting in a deficiency in ergosterol that causes fungal cell death. Use it until symptoms significantly improve.

Topical pyridones

Ciclopirox olamine 1% cream (Loprox)

Ciclopirox olamine interferes with the synthesis of DNA, RNA, and protein by inhibiting the transport of essential elements in fungal cells.

Topical benzylamines

Butenafine 1% cream (Mentax)

Butenafine inhibits squalene epoxidation, which, in turn, causes blockage of ergosterol biosynthesis (an essential component of fungal cell membranes), causing fungal cell growth to arrest.

Systemic azoles

Fluconazole (Diflucan)

Fluconazole is a synthetic oral antifungal (broad-spectrum bistriazole) that selectively inhibits fungal cytochrome P-450 and sterol C-14 alpha-demethylation, which prevents the conversion of lanosterol to ergosterol, thereby disrupting cellular membranes. It has little affinity for mammalian cytochromes, which is believed to explain its low toxicity. Fluconazole is available as tablet for oral administration, as powder for oral suspension, and as a sterile solution for intravenous use. It has fewer adverse effects and better tissue distribution than older systemic imidazoles.

Itraconazole (Sporanox)

Itraconazole has fungistatic activity; it is a synthetic triazole antifungal agent that inhibits fungal cell growth by inhibiting the cytochrome P-450–dependent synthesis of ergosterol, a vital component of fungal cell membranes.

Ketoconazole (Nizoral)

Ketoconazole inhibits the synthesis of ergosterol (main sterol of fungal cell membranes), causing cellular components to leak; this results in cell death. It is rarely used because of effective alternative agents and the risk of hepatotoxicity.

Systemic allylamines

Terbinafine (Lamisil, Daskil)

Terbinafine has fungicidal activity; it is a synthetic allylamine derivative that inhibits squalene epoxidase, a key enzyme in sterol biosynthesis of fungi, resulting in a deficiency in ergosterol that causes fungal cell death. Use it until symptoms significantly improve.

Other systemic antifungals

Griseofulvin (Fulvicin)

Griseofulvin has fungistatic activity; fungal cell division is impaired by interfering with microtubules. It binds to keratin precursor cells. Keratin is gradually replaced by noninfected tissue, which is highly resistant to fungal invasions.

Topical azoles

Clotrimazole 1% cream (Mycelex, Lotrimin)

Clotrimazole is a nonabsorbable imidazole. It is a broad-spectrum synthetic antifungal agent that inhibits growth of fungus by altering cell membrane permeability, which causes fungal cell death. Therapy is directed at the underlying condition, with the goal of minimizing symptoms and preventing complications.

Ketoconazole topical (Nizoral)

Ketoconazole topical is an imidazole, broad-spectrum antifungal agent indicated for topical treatment of tinea corporis. It inhibits the synthesis of ergosterol (main sterol of fungal cell membranes), causing cellular components to leak; the result is cell death.

Miconazole topical (Monistat)

Miconazole damages the fungal cell-wall membrane by inhibiting the biosynthesis of ergosterol. Membrane permeability is increased, causing nutrients to leak and resulting in fungal cell death. Lotion is preferred in intertriginous areas. If cream is used, apply sparingly to avoid maceration effects.

Oxiconazole 1% cream (Oxistat)

Oxiconazole damages the fungal cell wall membrane by inhibiting the biosynthesis of ergosterol. Membrane permeability is increased, causing nutrients to leak, resulting in fungal cell death.

Sertaconazole 2% cream (Ertaczo)

Sertaconazole is a topical imidazole antifungal active against T rubrum, T mentagrophytes, and Epidermophyton floccosum.

Sulconazole 1% cream or solution (Exelderm)

Sulconazole is a broad-spectrum antifungal agent that inhibits the synthesis of ergosterol, causing cellular components to leak and resulting in fungal cell death.

Luliconazole (Luzu)

Luliconazole is an imidazole antifungal that alters the fungal cell membrane by interacting with 14-alpha demethylase (an enzyme necessary for conversion of lanosterol to ergosterol). It is indicated in adults and children aged 2 years or older for tinea corporis caused by the organisms Trichophyton rubrum and Epidermophyton floccosum. It is available as a 1% topical cream.

 

Questions & Answers

Overview

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)?

Presentation

What are the signs and symptoms of tinea corporis (ringworm)?

What are the potential complications of inflammation due to tinea corporis (ringworm)?

What are the characteristics of Majocchi granuloma 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 are the characteristics of tinea corporis (ringworm) gladiatorum?

What is tinea imbricata?

What are the clinical characteristics of tinea imbricata?

What is tinea incognito?

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?

DDX

What are the differential diagnoses for Tinea Corporis?

Workup

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)?

Treatment

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)?

How can tinea corporis (ringworm) recur?

How is the spread of tinea corporis infection (ringworm) prevented?

What is the recommended follow-up care for tinea corporis (ringworm)?

Medications

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?