Tinea cruris, a pruritic superficial fungal infection of the groin and adjacent skin, is the second most common clinical presentation for dermatophytosis. Tinea cruris is a common and important clinical problem that may, at times, be a diagnostic and therapeutic challenge.
Other Medscape articles on tinea infections include Tinea Barbae, Tinea Capitis, Tinea Corporis, Tinea Faciei, Tinea Nigra, Tinea Pedis, and Tinea Versicolor.
The most common etiologic agents for tinea cruris include Trichophyton rubrum and Epidermophyton floccosum; less commonly Trichophyton mentagrophytes and Trichophyton verrucosum are involved. Tinea cruris is a contagious infection transmitted by fomites, such as contaminated towels or hotel bedroom sheets, or by autoinoculation from a reservoir on the hands or feet (tinea manuum, tinea pedis, tinea unguium). The etiologic agents in tinea cruris produce keratinases, which allow invasion of the cornified cell layer of the epidermis. The host immune response may prevent deeper invasion. Risk factors for initial tinea cruris infection or reinfection include wearing tight-fitting or wet clothing or undergarments.
Dermatophytosis accounts for approximately 10-20% of all visits to dermatologists.[1]
International
Tinea cruris has a worldwide distribution but is found more commonly in hot humid climates.[2, 3]
Sex
Tinea cruris is 3 times more common in men than in women.
Age
Adults are affected by tinea cruris much more commonly than are children. However, the prevalence of several risk factors for tinea cruris, such as obesity and diabetes mellitus, is rapidly increasing among adolescents.[4]
The prognosis of tinea cruris is excellent with appropriate diagnosis and treatment; however, recurrence is likely if the groin region is not kept dry.
No mortality is associated with tinea cruris. Associated pruritus leads to morbidity resulting from lichenification, secondary bacterial infection, and irritant and allergic contact dermatitis caused by topically applied medications.
Educate patients about the risks of sharing sheets and undergarments with others and about the need to keep the groin region dry (see Deterrence/Prevention).
For patient education resources, visit the Skin Conditions and Beauty Center. Also, see the patient education article Ringworm on Body.
Patients with tinea cruris report pruritus and rash in the groin. A history of previous episodes of a similar problem usually is elicited. Additional historical information in patients with tinea cruris may include recently visiting a tropical climate, wearing tight-fitting clothes (including bathing suits) for extended periods, sharing clothing with others, participating in sports, or coexisting diabetes mellitus or obesity. Prison inmates, members of the armed forces, members of athletic teams, and people who wear tight clothing may be subject to independent or additional risk for dermatophytosis.
Tinea cruris manifests as a symmetric erythematous rash in the groin, as shown in the images below.
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Tinea cruris.
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Tinea cruris.
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Tinea cruris.
Large patches of erythema with central clearing are centered on the inguinal creases and extend distally down the medial aspects of the thighs and proximally to the lower abdomen and pubic area.
Scale is demarcated sharply at the periphery.
In acute tinea cruris infections, the rash may be moist and exudative.
Chronic infections typically are dry with a papular annular or arciform border and barely perceptible scale at the margin.
Central areas typically are hyperpigmented and contain a scattering of erythematous papules and a little scale.
The penis and scrotum typically are spared in tinea cruris; however, the infection may extend to the perineum and buttocks.
Secondary changes of excoriation, lichenification, and impetiginization may be present as a result of pruritus.
Chronic infections modified by the application of topical corticosteroids are more erythematous, less scaly, and may have follicular pustules.
Approximately one half of patients with tinea cruris have coexisting tinea pedis.
Erythematous-scale plaques and erythematous-liquenificated plaques were the most frequently found clinical types in an excellent Brazilian study.[6] T rubrum was the prevalent dermatophyte in 90% of the cases, followed by T tonsurans (6%) and T mentagrophytes (4%).
The dermatophyte T rubrum is the most common etiologic agent for tinea cruris.[5] In a Brazilian series, T rubrum was the prevalent dermatophyte in 90% of the tinea cruris cases, followed by T tonsurans (6%) and T mentagrophytes (4%).[6] Other organisms, including E floccosum and T verrucosum, cause an identical clinical condition. T rubrum and E floccosum infections are more apt to become chronic and noninflammatory, while infection by T mentagrophytes often is associated with an acute inflammatory clinical presentation.
Tinea cruris can become infected secondarily by candidal or bacterial organisms. In addition, the area can become lichenified and hyperpigmented in the setting of a chronic fungal infection.
Mistreatment of tinea cruris with topical steroids can result in exacerbation of the disease. Although patients may note initial relief of symptoms, the infection may spread.
Microscopic examination of a potassium hydroxide (KOH) wet mount of scales is diagnostic in tinea cruris. The procedure for KOH wet mount is as follows:
Clean the area with 70% alcohol.
Collect scales from the margin of the lesion; use a scalpel or the edge of a glass slide for this purpose. Cover the collected scales with a cover slip; allow a drop of KOH (10-15% wt/vol) to run under the cover slip.
The keratin and debris should dissolve after a few minutes. The process can be hastened by heating the slide or by the addition of a keratolytic or dimethyl sulfoxide to the KOH formulation.
The addition of 1 drop of lactophenol cotton blue solution to the wet mount preparation heightens the contrast and aids in the diagnosis.
Negative results on KOH preparation do not exclude fungal infection.
Scale culture is useful for fungal identification but is a more specific, albeit less sensitive, diagnostic test than KOH wet mount.
Growth on Mycosel or Sabouraud agar plates usually is sufficient within 3-6 weeks to allow specific fungal identification.
Negative KOH wet mount examination and cultures exclude other conditions in the differential diagnosis. If tinea cruris still is suggested, repeat the tests, several times if necessary.
Punch biopsy is diagnostic but has low sensitivity and low specificity. Using periodic acid-Schiff stain (fungal elements appear pink) or methenamine silver stains (fungal elements appear brown or black) on the processed tissue enhances the sensitivity of the biopsy procedure.
Wood lamp examination may be helpful to exclude erythrasma, which reveals coral red florescence of the affected area.
The images below demonstrate the appearance of tinea cruris using a variety of staining techniques.
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Tinea cruris (hematoxylin and eosin stain).
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Tinea cruris (periodic acid-Schiff stain, magnification X 20).
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Tinea cruris (Gomori methenamine-silver stain, magnification X 20).
Microscopic examination of hematoxylin and eosin–stained tissue sections reveals patterns of inflammation strongly suggestive of dermatophyte infection. The inflammation typically is perivascular; the epidermis exhibits spongiosis or a psoriasiform pattern of hyperplasia. Granulomatous dermatitis may accompany folliculitis.
Specific diagnostic findings include the presence of neutrophils in the cornified cell layer and the sandwich sign, in which fungal elements are sandwiched between 2 zones of differing structure within the cornified cell layer. The upper zone of the cornified cell layer has a typical basket-weave pattern of orthokeratosis, while the lower zone consists of more compact orthokeratosis and parakeratosis. The presence of spores and branching hyphae can be confirmed using periodic acid-Schiff or methenamine silver stains, but histologic examination provides no clues regarding the dermatophyte species.
Clinical cure of an uncomplicated tinea cruris infection usually can be achieved using topical antifungal agents of the imidazole or allylamine family.[8] Consider patients unable to use topical treatments consistently or with extensive or recalcitrant infection as candidates for systemic administration of antifungal therapy, which has been proven safe in immunocompetent persons.[9]
Prevention of tinea cruris reinfection is an essential component of disease management. Patients with tinea cruris often have concurrent dermatophyte infections of the feet and hands.
Treat all active areas of tinea cruris infection simultaneously to prevent reinfection of the groin from other body sites. Advise patients with tinea pedis to put on their socks before their undershorts to reduce the possibility of direct contamination. Advise patients with tinea cruris to dry the crural folds completely after bathing and to use separate towels for drying the groin and other parts of the body.
Recurrence of tinea cruris is common; therefore, it is of utmost importance to treat concurrent fungal infections and to keep the groin region dry to prevent recurrence of tinea cruris. Advise patients to dry the area after bathing, using a towel or a hair dryer.
Advise patients with tinea cruris to avoid wearing tight-fitting clothing to prevent moisture build-up. Advise patients with tinea cruris who are obese to lose weight. Advise patients to put on socks before undergarments to minimize the possibility of fungal transfer from the feet to the groin.
Antifungal powders, which have the added benefit of drying the region, may be helpful in preventing recurrence of tinea cruris.
To achieve the best results, particularly with follicular or extensive tinea cruris, the authors often recommend a combination of topical and systemic therapy.[10]
The two classes of antifungal medications used most commonly to treat tinea cruris are the azoles and the allylamines. Azoles inhibit the enzyme lanosterol 14-alpha-demethylase, an enzyme that converts lanosterol to ergosterol, which is an important component of the fungal cell wall. Membrane damage results in permeability problems and renders the fungus unable to reproduce. Allylamines inhibit squalene epoxidase, which is an enzyme that converts squalene to ergosterol, resulting in the accumulation of toxic levels of squalene in the cell and in cell death. Examples of both classes of antifungal agents are available for topical and systemic administration. Some data suggest that fungistatic azoles can be as effective as fungicidal allylamines.[11] Both may have depot effects in the stratum corneum.[12]
Studies have found terbinafine to be effective and well tolerated in children.[13] Terbinafine 1% emulsion gel was found to be more effective than ketoconazole 2% cream in the treatment of tinea cruris.[14]
There may be some advantage to giving itraconazole with whole milk to increase absorption.14 However, because of its metabolism, drug interactions with inhibitors of cytochrome P450 are possible.[15]
Haloprogin is an agent for use in the treatment of tinea cruris. It is prescription only and is available in 1% cream and solution/spray. It is not available in the United States.
Clinical Context:
Terbinafine is a synthetic allylamine derivative, which inhibits squalene epoxidase, a key enzyme in sterol biosynthesis in fungi that results in a deficiency of ergosterol, causing fungal cell death. It is a widely studied and effective topical or oral antifungal. The topical form is available without a prescription. Some clinicians reserve this drug for more widespread/resistant infections because of its broad coverage and increased cost. Studies have found this medication to be effective and well tolerated in children.
Clinical Context:
Butenafine is a potent antifungal related to the allylamines. It damages fungal cell membranes, causing fungal cell growth to arrest. It is available in 1% cream only.
Clinical Context:
Clotrimazole topical is often the first-line drug used in the treatment of tinea cruris. It is a broad-spectrum antifungal agent that inhibits yeast growth by altering cell membrane permeability, causing the death of fungal cells. Reevaluate the diagnosis if no clinical improvement after is seen after 4 weeks. It is available without a prescription in 1% cream, solution/spray, and lotion.
Clinical Context:
Miconazole 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. It is available without a prescription, and 2% cream, solution/spray, lotion, and powder forms are available. Lotion is preferred in intertriginous areas. If cream is used, apply sparingly to avoid maceration effects.
Clinical Context:
Ketoconazole topical comes as 2% cream. It is an imidazole broad-spectrum antifungal agent; it inhibits the synthesis of ergosterol, causing cellular components to leak, resulting in fungal cell death.
Clinical Context:
Econazole is effective in cutaneous infections. It interferes with RNA and protein synthesis and metabolism. It disrupts fungal cell wall permeability, causing fungal cell death.
Clinical Context:
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 for tinea cruris caused by the organisms Trichophyton rubrum and Epidermophyton floccosum in adults and children aged 12 years or older. It is available as a 1% topical cream.
Clinical Context:
Naftifine is a broad-spectrum antifungal agent and synthetic allylamine derivative; it may decrease the synthesis of ergosterol, which, in turn, inhibits fungal cell growth. It is available in 1% cream or solution. If no clinical improvement is seen after 4 weeks, reevaluate the patient.
Clinical Context:
Oxiconazole is a broad-spectrum antifungal agent. It inhibits the synthesis of ergosterol, causing cellular components to leak, resulting in fungal cell death. It is available in 1% cream or lotion.
Clinical Context:
Tolnaftate is a nonprescription medication used in the treatment of tinea cruris. It is available in 1% cream, solution/spray, and powder.
Clinical Context:
Ciclopirox is a synthetic broad-spectrum antifungal agent. It interferes with the synthesis of DNA, RNA, and protein by inhibiting the transport of essential elements in fungal cells. It is available by prescription only in 1% cream and lotion.
Clinical Context:
Itraconazole has fungistatic activity. It is a synthetic triazole antifungal agent that slows fungal cell growth by inhibiting cytochrome P450–dependent synthesis of ergosterol, a vital component of fungal cell membranes. It is a widely used and well-studied oral antifungal that can be used in the treatment of tinea cruris. Studies have shown that it is tolerated better than griseofulvin. Best results are noted 2-3 weeks after the end of treatment.
Clinical Context:
Sulconazole is a broad-spectrum antifungal agent. It inhibits the synthesis of ergosterol, causing cellular components to leak, resulting in fungal cell death. It is available as 1% cream or solution.
Clinical Context:
Griseofulvin has fungistatic activity. Fungal cell division is impaired by interfering with microtubules. It binds to keratin precursor cells. Keratin gradually is replaced by noninfected tissue, which is highly resistant to fungal invasions. It is less effective than itraconazole in the treatment of tinea cruris.
The mechanism of action usually involves inhibiting pathways (enzymes, substrates, transport) necessary for sterol/cell membrane synthesis or altering the permeability of the cell membrane (polyenes) of the fungal cell.
What is tinea cruris (jock itch)?What is the pathogenesis of tinea cruris (jock itch)?What is the prevalence of tinea cruris (jock itch) in the US?What is the global prevalence of tinea cruris (jock itch)?How does the prevalence of tinea cruris (jock itch) vary by sex?How does the prevalence of tinea cruris (jock itch) vary by age?What is the prognosis of tinea cruris (jock itch)?What is the mortality and morbidity associated with tinea cruris (jock itch)?What education about tinea cruris (jock itch) should patients receive?What are the risk factors for tinea cruris (jock itch)?What are the signs and symptoms of tinea cruris (jock itch)?Which physical findings suggest tinea cruris (jock itch)?Which organisms cause tinea cruris (jock itch)?What are possible complications of tinea cruris (jock itch)?What is the role of topical steroids in the treatment of tinea cruris (jock itch)?What conditions should be included in the differential diagnoses of tinea cruris (jock itch)?What are the differential diagnoses for Tinea Cruris?How is tinea cruris (jock itch) diagnosed?What is the role of biopsy in the diagnosis of tinea cruris (jock itch)?How does the appearance of tinea cruris (jock itch) vary based on staining technique?Which microscopic findings suggest tinea cruris (jock itch)?Which histologic findings are diagnostic of tinea cruris (jock itch)?What are the treatment options for tinea cruris (jock itch)?What are common comorbidities of tinea cruris (jock itch)?How is reinfection of tinea cruris (jock itch) prevented?What are dietary restrictions in the management of tinea cruris (jock itch)?How can recurrence of tinea cruris (jock itch) be prevented?How can tinea cruris (jock itch) be prevented?What is the role of antifungal powders in the prevention of tinea cruris (jock itch)?What may be indicated if initial treatment of tinea cruris (jock itch) is unsuccessful?How may the best results for the treatment of tinea cruris (jock itch) be achieved?Which antifungal medications are used to treat tinea cruris (jock itch)?What is the efficacy of antifungal medication for the treatment of tinea cruris (jock itch)?What is the role of haloprogin in the treatment of tinea cruris (jock itch)?Which medications in the drug class Antifungal agents are used in the treatment of Tinea Cruris?
Michael Wiederkehr, MD, Consulting Staff, Livingston Dermatology Associates; Consulting Staff, Comprehensive Dermatology and Laser Center
Disclosure: Nothing to disclose.
Coauthor(s)
Robert A Schwartz, MD, MPH, Professor and Head of Dermatology, Professor of Pathology, Professor of Pediatrics, Professor of Medicine, Rutgers New Jersey Medical School
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.
Lester F Libow, MD, Dermatopathologist, South Texas Dermatopathology Laboratory
Disclosure: Nothing to disclose.
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
Gregory J Raugi, MD, PhD, Professor, Department of Internal Medicine, Division of Dermatology, University of Washington at Seattle School of Medicine; Chief, Dermatology Section, Primary and Specialty Care Service, Veterans Administration Medical Center of Seattle
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