1lnea crurls a prurlLlc superflclal fungal lnfecLlon of Lhe groln and ad[acenL skln ls Lhe second mosL

common cllnlcal presenLaLlon for dermaLophyLosls 1lnea crurls ls a common and lmporLanL cllnlcal
problem LhaL may aL Llmes be a dlagnosLlc and LherapeuLlc challenge
Pathophysiology
The most common etiologic agents Ior tinea cruris include Trichophyton rubrum and
Epidermophyton floccosum; less commonly Trichophyton mentagrophytes and Trichophyton
verrucosum are involved. Tinea cruris is a contagious inIection transmitted by Iomites, such
as contaminated towels or hotel bedroom sheets, or by autoinoculation Irom a reservoir on
the hands or Ieet (tinea manuum, tinea pedis, tinea unguium). The etiologic agents in tinea
cruris produce keratinases, which allow invasion oI the corniIied cell layer oI the epidermis.
The host immune response may prevent deeper invasion. Risk Iactors Ior initial tinea cruris
inIection or reinIection include wearing tight-Iitting or wet clothing or undergarments.
Frequency
UnlteJ Stutex
Dermatophytosis accounts Ior approximately 10-20 oI all visits to dermatologists.
|1|

nternutlonul
Tinea cruris has a worldwide distribution but is Iound more commonly in hot humid
climates.
|2, 3|

[rtalityJ[rbidity
No mortality is associated with tinea cruris. Associated pruritus leads to morbidity resulting
Irom licheniIication, secondary bacterial inIection, and irritant and allergic contact dermatitis
caused by topically applied medications.
Sex
Tinea cruris is 3 times more common in men than in women.
Age
Adults are aIIected by tinea cruris much more commonly than are children. However, the
prevalence oI several risk Iactors Ior tinea cruris, such as obesity and diabetes mellitus, is
rapidly increasing among adolescents.
istory
Patients with tinea cruris report pruritus and rash in the groin. A history oI previous episodes
oI a similar problem usually is elicited. Additional historical inIormation in patients with
tinea cruris may include recently visiting a tropical climate, wearing tight-Iitting clothes
(including bathing suits) Ior extended periods, sharing clothing with others, participating in
sports, or coexisting diabetes mellitus or obesity. Prison inmates, members oI the armed
Iorces, members oI athletic teams, and people who wear tight clothing may be subject to
independent or additional risk Ior dermatophytosis.
Physical
Tinea cruris maniIests as a symmetric erythematous rash in the groin, as shown in the images
below.
Tinea cruris. Tinea cruris.
Tinea cruris.
O Large patches oI erythema with central clearing are centered on the inguinal creases
and extend distally down the medial aspects oI the thighs and proximally to the lower
abdomen and pubic area.
O Scale is demarcated sharply at the periphery.
O In acute tinea cruris inIections, the rash may be moist and exudative.
O Chronic inIections typically are dry with a papular annular or arciIorm border and
barely perceptible scale at the margin.
O Central areas typically are hyperpigmented and contain a scattering oI erythematous
papules and a little scale.
O The penis and scrotum typically are spared in tinea cruris; however, the inIection may
extend to the perineum and buttocks.
O Secondary changes oI excoriation, licheniIication, and impetiginization may be
present as a result oI pruritus.
O Chronic inIections modiIied by the application oI topical corticosteroids are more
erythematous, less scaly, and may have Iollicular pustules.
O Approximately one halI oI patients with tinea cruris have coexisting tinea pedis.
O Erythematous-scale plaques and erythematous-liqueniIicated plaques were the most
Irequently Iound clinical types in an excellent Brazilian study.
|5|
T rubrum was the
prevalent dermatophyte in 90 oI the cases, Iollowed by T tonsurans (6) and T
mentagrophytes (4).
auses
The dermatophyte T rubrum is the most common etiologic agent Ior tinea cruris.
|6|
In a
Brazilian series, T rubrum was the prevalent dermatophyte in 90 oI the tinea cruris cases,
Iollowed by T tonsurans (6) and T mentagrophytes (4).
|5|
Other organisms, including E
floccosum and T verrucosum, cause an identical clinical condition. T rubrum and E floccosum
inIections are more apt to become chronic and noninIlammatory, while inIection by T
mentagrophytes oIten is associated with an acute inIlammatory clinical presentation.
ifferentials
O Acanthosis Nigricans
O Candidiasis, Cutaneous
O Contact Dermatitis, Allergic
O Contact Dermatitis, Irritant
O Erythrasma
O Familial Benign Pemphigus (Hailey-Hailey Disease)
O Folliculitis
O Intertrigo
O Psoriasis, Plaque
O Seborrheic Dermatitis
aboratory Studies
O Microscopic examination oI a potassium hydroxide (KOH) wet mount oI scales is
diagnostic in tinea cruris. The procedure Ior KOH wet mount is as Iollows:
4 Clean the area with 70 alcohol.
4 Collect scales Irom the margin oI the lesion; use a scalpel or the edge oI a
glass slide Ior this purpose. Cover the collected scales with a cover slip; allow
a drop oI KOH (10-15 wt/vol) to run under the cover slip.
4 The keratin and debris should dissolve aIter a Iew minutes. The process can be
hastened by heating the slide or by the addition oI a keratolytic or dimethyl
sulIoxide to the KOH Iormulation.
4 The addition oI 1 drop oI lactophenol cotton blue solution to the wet mount
preparation heightens the contrast and aids in the diagnosis.
4 Negative results on KOH preparation do not exclude Iungal inIection.
4 Scale culture is useIul Ior Iungal identiIication but is a more speciIic, albeit
less sensitive, diagnostic test than KOH wet mount.
O Growth on Mycosel or Sabouraud agar plates usually is suIIicient within 3-6 weeks to
allow speciIic Iungal identiIication.
Procedures
O Negative KOH wet mount examination and cultures exclude other conditions in the
diIIerential diagnosis. II tinea cruris still is suggested, repeat the tests, several times iI
necessary.
O Punch biopsy is diagnostic but has low sensitivity and low speciIicity. Using periodic
acid-SchiII stain (Iungal elements appear pink) or methenamine silver stains (Iungal
elements appear brown or black) on the processed tissue enhances the sensitivity oI
the biopsy procedure.
O Wood lamp examination may be helpIul to exclude erythrasma, which reveals coral
red Ilorescence oI the aIIected area.
O The images below demonstrate the appearance oI tinea cruris using a variety oI
staining techniques. Tinea cruris (hematoxylin and
eosin stain). Tinea cruris (periodic acid-SchiII stain,
magniIication X 20). Tinea cruris (Gomori
methenamine-silver stain, magniIication X 20
istologic Findings
Microscopic examination oI hematoxylin and eosinstained tissue sections reveals patterns oI
inIlammation strongly suggestive oI dermatophyte inIection. The inIlammation typically is
perivascular; the epidermis exhibits spongiosis or a psoriasiIorm pattern oI hyperplasia.
Granulomatous dermatitis may accompany Iolliculitis.
SpeciIic diagnostic Iindings include the presence oI neutrophils in the corniIied cell layer and
the sandwich sign, in which Iungal elements are sandwiched between 2 zones oI diIIering
structure within the corniIied cell layer. The upper zone oI the corniIied cell layer has a
typical basket-weave pattern oI orthokeratosis, while the lower zone consists oI more
compact orthokeratosis and parakeratosis. The presence oI spores and branching hyphae can
be conIirmed using periodic acid-SchiII or methenamine silver stains, but histologic
examination provides no clues regarding the dermatophyte species.
Medical are
Clinical cure oI an uncomplicated tinea cruris inIection usually can be achieved using topical
antiIungal agents oI the imidazole or allylamine Iamily. Consider patients unable to use
topical treatments consistently or with extensive or recalcitrant inIection as candidates Ior
systemic administration oI antiIungal therapy, which has been proven saIe in
immunocompetent persons.
|8|

Prevention oI tinea cruris reinIection is an essential component oI disease management.
Patients with tinea cruris oIten have concurrent dermatophyte inIections oI the Ieet and
hands.
O Treat all active areas oI tinea cruris inIection simultaneously to prevent reinIection oI
the groin Irom other body sites.
O Advise patients with tinea pedis to put on their socks beIore their undershorts to
reduce the possibility oI direct contamination.
O Advise patients with tinea cruris to dry the crural Iolds completely aIter bathing and to
use separate towels Ior drying the groin and other parts oI the body.
ntifungal agents
Class Summary
The 2 classes oI antiIungal 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 oI the Iungal
cell wall. Membrane damage results in permeability problems and renders the Iungus unable
to reproduce. Allylamines inhibit squalene epoxidase, which is an enzyme that converts
squalene to ergosterol, resulting in the accumulation oI toxic levels oI squalene in the cell and
in cell death. Examples oI both classes oI antiIungal agents are available Ior topical and
systemic administration.
Studies have Iound terbinaIine to be eIIective and well tolerated in children.
|9|
TerbinaIine
1 emulsion gel was Iound to be more eIIective than ketoconazole 2 cream in the
treatment oI tinea cruris.
|10|

Ilew full drug lnformaLlon
Terbinafine {Lamisil]

Synthetic allylamine derivative, which inhibits squalene epoxidase, a key enzyme in sterol
biosynthesis in Iungi that results in a deIiciency oI ergosterol, causing Iungal cell death.
Widely studied and eIIective topical or oral antiIungal. Topical Iorm available without
prescription. Some clinicians reserve this drug Ior more widespread/resistant inIections
because oI its broad coverage and increased cost. Studies have Iound this medication to be
eIIective and well tolerated in children.
Ilew full drug lnformaLlon
Butenafine {entax]

Potent antiIungal related to the allylamines. Damages Iungal cell membranes causing Iungal
cell growth to arrest.
Available in 1 cream only.
Ilew full drug lnformaLlon
Cl[trimaz[le t[\ical

OIten, Iirst-line drug used in the treatment oI tinea cruris. Broad-spectrum antiIungal agent
that inhibits yeast growth by altering cell membrane permeability, causing death oI Iungal
cells. Reevaluate diagnosis iI no clinical improvement aIter 4 wk.
Available without a prescription. 1 cream, solution/spray, and lotion available.
Ilew full drug lnformaLlon
ic[naz[le {icatin, [nistat-Derm]

Damages Iungal cell wall membrane by inhibiting biosynthesis oI ergosterol. Membrane
permeability is increased causing nutrients to leak, resulting in Iungal cell death.
Available without a prescription, and 2 cream, solution/spray, lotion, and powder Iorms
available. Lotion is preIerred in intertriginous areas. II cream is used, apply sparingly to
avoid maceration eIIects.
Ilew full drug lnformaLlon
Ket[c[naz[le t[\ical {Niz[ral]

2 cream. Imidazole broad-spectrum antiIungal agent; inhibits synthesis oI ergosterol,
causing cellular components to leak, resulting in Iungal cell death.
Ilew full drug lnformaLlon
Ec[naz[le {S\ectaz[le]

EIIective in cutaneous inIections. InterIeres with RNA and protein synthesis and metabolism.
Disrupts Iungal cell wall permeability, causing Iungal cell death.
Ilew full drug lnformaLlon
Naftifine {Naftin]

Broad-spectrum antiIungal agent and synthetic allylamine derivative; may decrease the
synthesis oI ergosterol, which in turn inhibits Iungal cell growth
Available in 1 cream or solution.
II no clinical improvement aIter 4 wk, reevaluate patient.
Ilew full drug lnformaLlon
Uxic[naz[le {Uxistat]

Broad-spectrum antiIungal agent. Inhibits synthesis oI ergosterol, causing cellular
components to leak, resulting in Iungal cell death.
1 cream or lotion.
Ilew full drug lnformaLlon
T[lnaftate {Tinactin]

Nonprescription medication used in the treatment oI tinea cruris. Available in 1 cream,
solution/spray, and powder.
Hal[\r[gin {Hal[tex]

Agent Ior use in the treatment oI tinea cruris. Prescription only. Available in 1 cream and
solution/spray.
Ilew full drug lnformaLlon
Cicl[\ir[x {L[\r[x]

Synthetic broad-spectrum antiIungal agent. InterIeres with synthesis oI DNA, RNA, and
protein by inhibiting the transport oI essential elements in Iungal cells. Prescription only.
Available in 1 cream and lotion.
Ilew full drug lnformaLlon
Itrac[naz[le {S\[ran[x]

Fungistatic activity. Synthetic triazole antiIungal agent that slows Iungal cell growth by
inhibiting cytochrome P450-dependent synthesis oI ergosterol, a vital component oI Iungal
cell membranes. Widely used and well-studied oral antiIungal that can be used in the
treatment oI tinea cruris. Studies have shown that it is tolerated better than griseoIulvin. Best
results are noted 2-3 wk aIter the end oI treatment.
Ilew full drug lnformaLlon
Sulc[naz[le {Exelderm]

Broad-spectrum antiIungal agent. Inhibits synthesis oI ergosterol, causing cellular
components to leak, resulting in Iungal cell death.
1 cream or solution.
Ilew full drug lnformaLlon
Crise[fulvin {Fulvicin-UJF, Crifulvin-V]

Fungistatic activity. Fungal cell division is impaired by interIering with microtubule. Binds to
keratin precursor cells. Keratin gradually is replaced by noninIected tissue, which is highly
resistant to Iungal invasions.
Less eIIective than itraconazole in treatment oI tinea cruris
dult osing & Uses
D[sing F[rms & Strengtbs
tablet
O mg
oral granules
O mg
O mg
Unycb[myc[sis
Fingernail: 1 tablet (250 mg) PO qD x 6 weeks
Toenail: 1 tablet (250 mg) PO qD x 12 weeks
Tinea Ca\itis
~35 kg: 250 mg PO qD x 6 weeks
Renal Im\airment
Clcr 50 mL/min: Use not recommended
He\atic Im\airment
Chronic or active liver disease: use not recommended