Tinea Cruris

Background

Tinea cruris (sometimes referred to as jock itch), a pruritic superficial fungal infection of the groin and adjacent skin, is the second most common clinical presentation for dermatophytosis. It is most commonly caused by Trichophyton rubrum or Epidermophyton floccosum; less commonly, Trichophyton mentagrophytes or Trichophyton verrucosum is involved. Trichophyton indotineae (formerly classified as T mentagrophytes genotype VIII) was first delineated in southern Asia in 2014 and is spreading worldwide.^[1] Tinea cruris is a common and important clinical problem that may, at times, be a diagnostic and therapeutic challenge. Treatment is a particular concern when T indotineae is involved.

Uncomplicated tinea cruris can usually be successfully treated with topical antifungal agents. (See Treatment.) Patients who are unable to use topical treatments consistently or who have extensive or recalcitrant infection may considered candidates for systemic antifungal therapy. Prevention of reinfection is an essential component of disease management.

Other types of tinea include tinea barbae, tinea capitis, tinea corporis, tinea faciei, tinea nigra, tinea pedis, and tinea versicolor.

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Pathophysiology

Tinea cruris is a contagious infection transmitted by fomites (eg, from contaminated towels or hotel bedroom sheets) or by autoinoculation from a reservoir on the hands or feet (eg, tinea manuum, tinea pedis, or 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.^[2]  Tinea cruris may be spread from person to person, especially when it is caused by T indotineae, and sexual transmission is suggested.^[1]

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Etiology

The dermatophyte T rubrum is the most common etiologic agent for tinea cruris,^[3]  though T mentagrophytes is becoming increasingly prevalent in this setting.^[4] In a 2001 Brazilian series, T rubrum was the prevalent dermatophyte in 90% of the tinea cruris cases, followed by T tonsurans (6%) and T mentagrophytes (4%).^[5]  T indotineae can cause refractory tinea cruris.^[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, whereas T mentagrophytes infection is often associated with an acute inflammatory clinical presentation.

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Epidemiology

United States and international statistics

In a 2004 study by Foster et al, dermatophytosis accounted for approximately 10-20% of all visits to dermatologists in the United States from 1999 to 2002.^[7]  For the period from 2005 to 2014, dermatophyte infections were responsible for 4,981,444 outpatient visits in the United States.^[4] In a 2024 study using data from a major US commercial laboratory (Labcorp), Zarzeka et al reported 2026 cases of tinea cruris for the period from March 1, 2019, to March 1, 2023^[8] ; T rubrum was the most commonly isolated pathogen (77.6%), followed by T tonsurans (14.5%).

Tinea cruris has a worldwide distribution but is found more commonly in hot humid climates.^{[9, 10]}  A study from Iran found that tinea cruris was the second most common dermatophyte infection (after tinea corporis) in Tehran for the period from 2010 to 2020.^[11]

Age- and sex-related demographics

Adults are affected by tinea cruris much more commonly than children are. However, the prevalence of several risk factors for tinea cruris, such as obesity and diabetes mellitus, is rapidly increasing among adolescents.^[12]

Tinea cruris is three times more common in men than in women.^[8]

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Prognosis

The prognosis for patients with 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.

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Patient Education

Efforts should be made to educate patients about the risks of sharing sheets and undergarments with others and about the need to keep the groin region dry (see Prevention).

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History

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.

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Physical Examination

Tinea cruris manifests as a symmetric erythematous rash in the groin (see the images below). 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.

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Tinea cruris.

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Tinea cruris.

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Tinea cruris.

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.

In an excellent Brazilian study from 2001, erythematous-scale plaques and erythematous-liquenificated plaques were the most frequently found clinical types.^[5] T rubrum was the prevalent dermatophyte in 90% of the cases, followed by T tonsurans 6%) and T mentagrophytes (4%).

Approximately one half of patients with tinea cruris have coexisting tinea pedis.

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Complications

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.

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Laboratory Studies

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, using a scalpel or the edge of a glass slide; cover the collected scales with a cover slip, then 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 adding a keratolytic or dimethyl sulfoxide to the KOH formulation
• The addition of one 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.

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Procedures

Negative KOH wet mount examination and cultures exclude other conditions in the differential diagnosis. If tinea cruris is still suggested, the tests should be repeated, several times if necessary.

Punch biopsy is diagnostic but has low sensitivity and low specificity. Using periodic acid-Schiff (PAS) stain (fungal elements appear pink; see the first image below) or methenamine silver stains (fungal elements appear brown or black; see the second image below) on the processed tissue enhances the sensitivity of the biopsy procedure.

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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).

Wood lamp examination may be helpful to exclude erythrasma, which reveals coral-red florescence of the affected area.

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Histologic Findings

Microscopic examination of hematoxylin and eosin–stained tissue sections (see the image below) 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.

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Tinea cruris (hematoxylin and eosin stain).

Specific diagnostic findings include the presence of neutrophils in the cornified cell layer and the sandwich sign, in which fungal elements are sandwiched between two 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, whereas the lower zone consists of more compact orthokeratosis and parakeratosis. The presence of spores and branching hyphae can be confirmed with PAS or methenamine silver stains, but histologic examination provides no clues regarding the dermatophyte species.

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Medical Care

Clinical cure of an uncomplicated tinea cruris infection usually can be achieved by using topical antifungal agents of the imidazole family (eg, clotrimazole,^[14] fluconazole, miconazole, ketoconazole, itraconazole, and sertaconazole) or the allylamine family (eg, terbinafine,^[15] butenafine, and naftifine^{[16, 17]} ):

• 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.^[18]  Both may have depot effects in the stratum corneum.^[19]

Patients who are unable to use topical treatments consistently or who have extensive or recalcitrant infection may be considered candidates for systemic administration of antifungal therapy, which has been shown to be safe in immunocompetent persons.^[20]  To achieve the best results, particularly with follicular or extensive tinea cruris, the authors often recommend a combination of topical and systemic therapy.^[21]  

Studies have found terbinafine to be effective and well tolerated in children.^[22]  A comparative study found terbinafine 1% emulsion gel to be more effective than ketoconazole 2% cream in the treatment of tinea cruris.^[23]  The emerging pathogen T indotineae has shown significant resistance to terbinafine^[24] and thus may be best treated with a combination of oral and topical antifungals.^[25] Itraconazole has been recommended for this organism.^[26]

There may be some advantage to giving itraconazole with whole milk to increase absorption.^[19]  However, because of its metabolism, drug interactions with inhibitors of cytochrome P450 are possible.^[27]

The growing frequency of antifungal-resistant dermatophyte infections is a matter of global concern. Accordingly, obtaining mycologic confirmation before initiating treatment, when feasible, should be considered best practice.^[28] A high index of suspicion for resistant dermatophyte infections should be maintained, in conjunction with antifungal stewardship efforts.

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.

All active areas of tinea cruris infection should be treated simultaneously so as to prevent reinfection of the groin from other body sites. Patients with tinea pedis should be advised to put on their socks before their undershorts so as to reduce the possibility of direct contamination. Patients with tinea cruris should be advised to dry the crural folds completely after bathing and to use separate towels for drying the groin and other parts of the body.

If initial treatment of tinea cruris is unsuccessful, repeat scraping or culture (see Workup) may be indicated.

Emerging patterns of resistance will dictate the use of alternative agents to treat tinea cruris.^[29]

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Prevention

Given that recurrence of tinea cruris is common, it is of the utmost importance to treat concurrent fungal infections and to keep the groin region dry to prevent tinea cruris from returning. Patients should be advised to dry the area after bathing, using a towel or a hair dryer.

Patients with tinea cruris should be advised to avoid wearing tight-fitting clothing so as to prevent moisture buildup. Those who are obese should be advised to lose weight. Those who had tinea pedis should make a point of putting on socks before undergarments so as 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.

Given that tinea cruris due to T indotineae may be spread from person to person, with sexual transmission suggested, suitable precautions should be considered.^[1]

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Terbinafine (Lamisil)

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Itraconazole (Onmel, Sporanox, Sporanox Oral Solution)

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Griseofulvin (Grifulvin V (DSC), Gris-PEG (DSC))

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Terbinafine topical (Lamisil AT topical)

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Butenafine (Lotrimin Ultra, Mentax, Mentax-TC)

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Naftifine (Naftin)

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Ciclopirox (Loprox, Penlac)

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Sulconazole (Exelderm)

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Luliconazole (Luzu)

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Oxiconazole (Oxistat)

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Econazole topical (Ecoza)

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Miconazole topical (Cavilon Antifungal Cream, Desenex, Fungoid Tincture)

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Ketoconazole topical (Extina (DSC), Ketozole, Nizoral Anti-Dandruff Shampoo)

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Clotrimazole topical (Gyne Lotrimin, Lotrimin, Lotrimin AF)

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Tolnaftate (Absorbine, Aftate, Barielle Fungus Rx)

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