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Background

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.
Pathophysiology
Epidemiology
Frequency
United States
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]
Prognosis
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.
Patient Education
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.

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.
Physical Examination
Tinea cruris manifests as a symmetric erythematous rash in the groin, as
shown in the images below.

Tinea cruris.
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Tinea cruris.
View Media Gallery
Tinea cruris.
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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%).
Causes
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.
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.

Also consider histiocytosis X [7] and psoriasis inversus.


Differential Diagnoses
 Acanthosis Nigricans
 Allergic Contact Dermatitis
 Cutaneous Candidiasis
 Erythrasma
 Familial Benign Pemphigus (Hailey-Hailey Disease)
 Folliculitis
 Intertrigo
 Irritant Contact Dermatitis
 Plaque Psoriasis
 Seborrheic Dermatitis
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; 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.
Procedures
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.

Tinea cruris (hematoxylin


and eosin stain).
View Media Gallery

Tinea cruris (periodic acid-


Schiff stain, magnification X 20).
View Media Gallery
Tinea cruris (Gomori
methenamine-silver stain, magnification X 20).
View Media Gallery
Histologic Findings
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.
Medical Care
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.
Diet
Recommend weight loss for patients who are obese and have tinea cruris.
Prevention
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.
Long-Term Monitoring
Repeat scraping or culture may be indicated if initial treatment of tinea
cruris is unsuccessful.
Medication Summary
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.
Antifungal agents
Class Summary
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.
Terbinafine (Lamisil)
 View full drug information
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.

Dosage Forms & Strengths


tablet
 250mg
packet, oral granules
 125mg
 187.5mg

Onychomycosis
250 mg (1 tablet) PO daily for 6 weeks (fingernail) or 12 weeks (toenail)
Tinea Pedis (Off-label)
250 mg/day PO in single dose or divided q12hr for 2-6 weeks
Tinea Corporis, Tinea Cruris
250 mg/day PO in single dose or divided q12hr for 2-4 weeks
Sporotrichosis, Lymphocutaneous and cutaneous (Off-label)
500 mg/day PO q12hr for 2-6 weeks; treat for additional 2-4 weeks after
resolution of all lesions (resolution may take 3-6 months)
Dosing Modifications
Renal impairment: Use not recommended if CrCl <50 mL/min
Hepatic impairment: Use contraindicated in chronic or active liver disease

Butenafine (Mentax)
 View full drug information
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.
Clotrimazole topical (Lotrimin, Mycelex)
 View full drug information
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.
Miconazole (Micatin, Monistat-Derm)
 View full drug information
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.
Ketoconazole topical (Nizoral)
 View full drug information
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.
Econazole topical (Ecoza)
 View full drug information
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.
Luliconazole (Luzu)
 View full drug information
Luliconazole is available as a 1% topical cream administered once daily for
1 week. It 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 corporis.
Naftifine (Naftin)
 View full drug information
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.
Oxiconazole (Oxistat)
 View full drug information
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.
Tolnaftate (Tinactin)
 View full drug information
Tolnaftate is a nonprescription medication used in the treatment of tinea
cruris. It is available in 1% cream, solution/spray, and powder.
Ciclopirox (Loprox)
 View full drug information
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.
Itraconazole (Sporanox)
 View full drug information
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.
Sulconazole (Exelderm)
 View full drug information
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.
Griseofulvin (Fulvicin-U/F, Grifulvin-V)
 View full drug information
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.

1. Widaty, Sandra dan Unandar Budimulja. Dermatofitosis. Dalam : Menaldi Sri


Linuwih SW, Bramono Kusmarinah, Indriatmi Wresti, editor. Ilmu Penyakit Kulit dan
Kelamin. Edisi 7. Cetakan Keempat. Jakarta : Badan Penerbit FKUI; 2017. Hal 111-
116
2. Andrews Shari, dkk. Tinea in Emergency Medicine. Medscape ; 2017
https://emedicine. medscape.com/article/787217-overview
3. Sahoo, Alok Kumar, dkk. Management of Tinea Corporis, Tinea Cruris, and Tinea
Pedis: A Comprehensive Review. NCBI: Indian Dermatology; 2016; 7(2): 77–86
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4804599/
4. Yosella, Tanti. Diagnosis and Treatment of Tinea Cruris. Dalam : J Majority. Jurnal
Kedokteran UNILA.Volume 4 nomor 2. 2015. Lampung : UNILA;2015. Hal 122-127
5. Wiederkehr, Michael. Tinea Cruris. Medscape; 2017.
https://emedicine.medscape.com/article/1091806-overview
6.
7.

For isolated plaques on the glabrous skin, topical allylamines, imidazoles, tolnaftate, butenafine, or
ciclopirox are effective. Most are applied twice daily for 2–4 weeks. Oral antifungal agents are
reserved for widespread or more inflammatory eruptions. Comparative studies in adults show that
terbinafine 250 mg daily for 2–4 weeks, itraconazole 200 mg daily for 1 week, and fluconazole 150–
300 mg weekly for 4–6 weeks are preferable over griseofulvin 500 mg dailyuntil cure is reached.73
Safe and effective regimens for children include terbinafine 3–6 mg/kg/day for 2 weeks, itraconazole
5 mg/kg/day for 1 week, and ultramicrosize griseofulvin 10–20 mg/ kg/day for up to 2–4 weeks.

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