You are on page 1of 6

http://emedicine.medscape.

com/article/1091684-overview, akses 12 oktober 2013

Background
Tinea pedis has afflicted humanity for centuries, so it is perhaps surprising that the condition was not
described until Pellizzari did so in 1888.[1] The first report of tinea pedis was in 1908 by Whitfield, who, with
Sabouraud, believed that tinea pedis was a very rare infection caused by the same organisms that
produce tinea capitis.
Tinea pedis is the term used for a dermatophyte infection of the soles of the feet and the interdigital
spaces. Tinea pedis is most commonly caused byTrichophyton rubrum, a dermatophyte initially endemic
only to a small region of Southeast Asia and in parts of Africa and Australia. Interestingly, tinea pedis was
not noted in these areas then, possibly because these populations did not wear occlusive footwear. The
colonization of the T rubrum endemic regions by European nations helped to spread the fungus
throughout Europe. Wars with accompanying mass movements of troops and refugees, the general
increase in available means of travel, and the rise in the use of occlusive footwear have all combined to
make T rubrum the world's most prevalent dermatophyte.[2]
The first reported case of tinea pedis in the United States was noted in Birmingham, Alabama, in the
1920s. World War I troops returning from battle may have transported T rubrum to the United States.

PATOFISIOLOGI
T rubrum, Trichophyton mentagrophytes, and Epidermophyton floccosum most commonly cause tinea
pedis, with T rubrum being the most common cause worldwide. Trichophyton tonsurans has also been
implicated in children. Nondermatophyte causes include Scytalidium dimidiatum, Scytalidium hyalinum,
and, rarely, Candida species.
Using enzymes called keratinases, dermatophyte fungi invade the superficial keratin of the skin, and the
infection remains limited to this layer. Dermatophyte cell walls also contain mannans, which can inhibit the
body's immune response. T rubrum in particular contains mannans that may reduce keratinocyte
proliferation, resulting in a decreased rate of sloughing and a chronic state of infection.
Temperature and serum factors, such as beta globulins and ferritin, appear to have a growth-inhibitory
effect on dermatophytes; however, this pathophysiology is not completely understood. Sebum also is
inhibitory, thus partly explaining the propensity for dermatophyte infection of the feet, which have no
sebaceous glands. Host factors such as breaks in the skin and maceration of the skin may aid in
dermatophyte invasion. The cutaneous presentation of tinea pedis is also dependent on the host's
immune system and the infecting dermatophyte.

EPIDEMIOLOGI
Frequency
International
Tinea pedis is thought to be the world's most common dermatophytosis. Reportedly, 70% of the
population will be infected with tinea pedis at some time.

Mortality/Morbidity
Tinea pedis is not associated with significant mortality or morbidity.

Race
Tinea pedis has no predilection for any racial or ethnic group.

Sex
Tinea pedis more commonly affects males compared with females.

Age
The prevalence of tinea pedis increases with age. Most cases occur after puberty. Childhood tinea pedis
is rare.

MEDICATION
Tinea pedis can be treated with topical or oral antifungals or a combination of both. [7, 8, 9] Topical agents are
used for 1-6 weeks, depending on manufacturers' recommendations. A patient with chronic hyperkeratotic
(moccasin) tinea pedis should be instructed to apply medication to the bottoms and sides of his or her
feet. For interdigital tinea pedis, even though symptoms may not be present, a patient should apply the
topical agent to the interdigital areas and to the soles because of the likelihood of plantar-surface
infection.
Recurrence of tinea pedis is often due to a patient's discontinuance of medication after symptoms abate.
A simple strategy to increase a patient's compliance is to prescribe a large quantity of topical medicine,
which may motivate a patient to continue use until the entire tube is empty.
Moccasin-type tinea pedis is often recalcitrant to topical antifungals alone, owing to the thickness of the
scale on the plantar surface. The concomitant use of topical urea or other keratolytics with topical
antifungals should improve the response to topical agents. In addition, for moccasin tinea pedis caused
byScytalidium species, Whitfield solution, containing benzoic and salicylic acids, can be beneficial.
However, patients with extensive chronic hyperkeratotic tinea pedis or inflammatory/vesicular tinea pedis
usually require oral therapy, as do patients with concomitant onychomycosis, [10] diabetes,[11] peripheral
vascular disease, or immunocompromising conditions.

Topical imidazoles
Class Summary
Effective in all forms of tinea pedis but are excellent treatments for interdigital tinea pedis because they
are effective against dermatophytes and Candida. Some of these drugs (eg, econazole) also have
antibacterial activity.
View full drug information

Clotrimazole 1% (Mycelex, Lotrimin)

Broad-spectrum antifungal agent that inhibits yeast growth by altering cell-membrane permeability,
causing death of fungal cells. Reevaluate diagnosis if no clinical improvement after 4 wk.
View full drug information

Econazole (Spectazole Topical)


Effective in cutaneous infections. May interfere with RNA and protein synthesis and metabolism. Disrupts
cell membrane permeability, causing death of fungal cells.
View full drug information

Ketoconazole topical (Nizoral)


Imidazole broad-spectrum antifungal agent; inhibits synthesis of ergosterol, causing cellular components
to leak, resulting in death of fungal cells.
View full drug information

Miconazole topical (Monistat)


Damages fungal cell wall membrane by inhibiting biosynthesis of ergosterol. Membrane permeability is
increased, causing nutrients to leak out, resulting in fungal cell death. The 2% lotion is preferred in
intertriginous areas. If the 2% cream is used, apply sparingly to avoid maceration effects.
View full drug information

Oxiconazole 1% cream (Oxistat)


Damages fungal cell wall membrane by inhibiting biosynthesis of ergosterol. Membrane permeability is
increased, causing nutrients to leak out, resulting in death of fungal cells.
View full drug information

Sertaconazole nitrate cream (Ertaczo)


Topical imidazole antifungal active against T rubrum, T mentagrophytes, and E floccosum. Indicated for
tinea pedis.

Topical pyridones
Class Summary
Broad-spectrum agents with antidermatophytic, antibacterial, and anticandidal activity and are therefore
useful in all forms of tinea pedis but especially effective in interdigital tinea pedis.
View full drug information

Ciclopirox 1% cream (Loprox)


Interferes with synthesis of DNA, RNA, and protein by inhibiting transport of essential elements in fungal
cells.

Topical allylamines
Class Summary
Effective in treating all forms of tinea pedis. In vitro, these agents have demonstrated potent activity
against dermatophyte fungi, so they are useful in treating patients with refractory tinea pedis (eg, chronic
hyperkeratotic). Terbinafine 1% (Lamisil) has been shown to be effective in some patients with interdigital
tinea pedis with only 1 wk of treatment. Patients with chronic hyperkeratotic tinea pedis generally require
4 wk of treatment.
View full drug information

Naftifine 1% cream and gel (Naftin)


Broad-spectrum antifungal agent and synthetic allylamine derivative; may decrease synthesis, which, in
turn, inhibits growth of fungal cells.
View full drug information

Terbinafine topical (Lamisil)


Inhibits squalene epoxidase, which decreases ergosterol synthesis, causing death of fungal cells. Use
until symptoms significantly improve. Duration of treatment should be >1 wk but not >4 wk.

Topical benzylamines
Class Summary
Sometimes classified as a subset of allylamines. Useful for treating patients with refractory tinea pedis
(eg, chronic hyperkeratotic). Have been shown to be effective in some patients with interdigital tinea pedis
with only 1 wk of treatment.[12]
View full drug information

Butenafine (Mentax)
Damages fungal cell membranes, arresting growth of fungal cells.

Oral antimycotics

Class Summary
Should be considered in patients with extensive chronic hyperkeratotic or inflammatory/vesicular tinea
pedis. Could also be used for patients with disabling disease, patients in whom topical treatments have
failed, patients with diabetes or peripheral vascular disease, and patients with immunocompromising
conditions.
View full drug information

Itraconazole (Sporanox)
Fungistatic activity. Synthetic triazole antifungal agent that slows fungal cell growth by inhibiting
cytochrome P-450dependent synthesis of ergosterol, a vital component of fungal cell membranes.
View full drug information

Terbinafine (Lamisil, Daskil)


Inhibits squalene epoxidase, which decreases ergosterol synthesis, causing death of fungal cells. Use
until symptoms significantly improve.
View full drug information

Fluconazole (Diflucan)
Synthetic oral antifungal (broad-spectrum bistriazole) that selectively inhibits fungal cytochrome P-450
and sterol C-14 alpha-demethylation.

Dermatological agents
Class Summary
May use to supplement antimycotic agents in certain clinical situations.

Aluminum acetate (Otic Domeboro, Burow's Solution)


Drying agent for vesicular tinea pedis. Dissolve aluminum acetate tablets in water to produce a 1:10-40
solution.
View full drug information

Ammonium lactate lotion (Lac Hydrin)


Used to decrease scaling in patients with hyperkeratotic soles. Contains lactic acid, an alpha hydroxy acid
that has keratolytic action and thus facilitates release of comedones. Causes disadhesion of corneocytes.
Available in 12% and 5% strengths. Use 12% lotion.
View full drug information

Urea, topical (Carmol-40, Keralac)


Used to decrease scaling in patients with hyperkeratotic soles. Promotes hydration and removal of excess
keratin by dissolving the intracellular matrix. Available in 10-40% concentration.

Prognosis
The type of tinea pedis infection and underlying conditions (eg, immunosuppression, diabetes) affect the
prognosis; however, with appropriate treatment, the prognosis is generally good.

You might also like