Background

Tinea faciei is a superficial dermatophyte infection limited to the glabrous skin of the face.[1] In pediatric and female patients, the infection may appear on any surface of the face, including the upper lip and chin. In men, the condition is known as tinea barbae when a dermatophyte infection of bearded areas occurs.

Pathophysiology
Keratinophilic fungi, or dermatophytes, are responsible tinea faciei. Dermatophytes release several enzymes, including keratinases, which allow them to invade the stratum corneum of the epidermis. Infection caused by zoophilic dermatophytes is usually associated with inflammatory reactions that are more severe than those due to anthropophilic fungi.

Epidemiology
Frequency International

Tinea faciei is not an uncommon disease. It occurs worldwide. However, as with other cutaneous fungal infections, it is more common in tropical regions with high temperatures and humidity.[2, 3, 4, 5] Tinea faciei was shown to represent approximately 19% of all superficial fungal infections in the pediatric population with dermatomycoses.[6]
Mortality/Morbidity

Scarring may occur in patients with Trichophyton schoenleinii infection; this is extremely rare.
Sex

Some authors suggest that females may be affected more frequently than males, but the difference is probably semantic. In females, dermatophyte infection of the face is more likely to be diagnosed as tinea faciei, whereas many infections that occur in similar locations in men are diagnosed as tinea barbae. Data indicate a female-to-male ratio of 1.06:1.[7]
Age

Tinea faciei may appear in persons of any age, with 2 peaks of disease incidence. One peak involves children, who constitute a large group of patients because of their frequent direct contact with pets. Tinea faciei is commonly noted as a dermatosis that occurs after holidays; it is diagnosed more frequently in children after they spend their holidays in rural areas, where they may come into contact with animals when they play. Several cases are also reported in neonates[8, 9, 10] ; these patients may acquire the infection from siblings or contact with pets. The other peak occurs in those aged 20-40 years.

History

Tinea faciei is frequently acquired from pets in the home, but it can also be spread from individuals with dermatophyte infection elsewhere on the body. Tinea faciei may resemble other dermatoses, such as cutaneous lupus erythematosus, polymorphous light eruption, and allergic contact dermatitis.[11, 12]

Physical

Because of the complex anatomy of the face, atypical features are more frequently found on the glabrous skin than the typical patches of tinea corporis. Single or multiple erythematous patches without annular structure often resemble other dermatoses; delayed or missed diagnosis may result. Lesions are almost always pruritic. Typical signs of dermatophyte infection of the glabrous skin, similar to those of tinea corporis, may be present. These signs include annular or serpiginous erythematous scaling patches with an active border composed of papules, vesicles, and/or crusts. The most common locations are the cheeks, followed by the nose, periorbital area, chin, and forehead. Some patients may have multiple lesions present in different areas

of the face. See the images below. Multiple lesions on the face caused by Microsporum canis infection in a patient who also has tinea capitis.

Erythematous scaling lesion on the cheek. In as many as 70% of patients with tinea faciei, various other dermatoses are considered. o Tinea faciei is the most frequently misdiagnosed entity among cutaneous fungal infections. o The atypical clinical features and incognito presentations support the separation of this disease from tinea corporis. o Occasionally, tinea faciei may simultaneously occur with other forms of dermatophyte infections, especially tinea capitis and tinea corporis.

Causes
The causative agents of tinea faciei vary according to geographic regions.

Generally, animal reservoirs of zoophilic dermatophytes, especially Microsporum canis, are global among pets and livestock.[13, 2] In Asia, Trichophyton mentagrophytes and Trichophyton rubrum are common.[14, 15] In contrast, in North America Trichophyton tonsurans is the main pathogen isolated.

Differentials

Candidiasis, Cutaneous Contact Dermatitis, Allergic Contact Dermatitis, Irritant Granuloma Annulare Lupus Erythematosus, Acute Lupus Erythematosus, Bullous Lupus Erythematosus, Discoid Lupus Erythematosus, Drug-Induced Lupus Erythematosus, Subacute Cutaneous Neonatal Lupus Erythematosus Perioral Dermatitis Pityriasis Alba Pityriasis Rosea Rosacea Sarcoidosis Seborrheic Dermatitis Syphilis

Laboratory Studies

Even in the best mycology laboratories, as many as 30% of culture results may be negative, particularly in chronic infections. Mycologic investigation is essential in the diagnosis of tinea faciei. It includes direct microscopic examination for hyphal elements and culturing. The collection of the surface scrapings is important for laboratory studies. The material should be obtained from the border of the lesions where the more severe inflammatory reaction occurs and where more fungal elements are present. Direct microscopic examination is the easiest mycologic procedure. o Scrapings are placed in 10-20% potassium hydroxide (KOH) solution, usually with the addition of dimethyl sulfoxide (DMSO). The latter helps to dissolve background keratinocytes to enable visualization of the fungal elements. o After warming the slide for a short time, the specimen is examined with a light microscope. o Some authors suggest detection is enhanced with special stains, such as chlorazol black E, Parker blue-black ink, or Swartz-Lamkin stain. Culturing allows the identification of the causative pathogen.

Culturing is performed routinely with Sabouraud agar and the addition of cycloheximide and chloramphenicol. These substances inhibit the growth of bacteria and other contaminants. o After 3-4 weeks of incubation, the final identification is based on morphologic and microscopic findings in the colonies. Dermatophytes may be diagnosed by using special media for rapid detection. This media contains a color indicator that changes from yellow to red with the growth of dermatophytes after a few days of incubation.

Histologic Findings
Histologic examination may occasionally be useful for establishing the diagnosis, but it is usually unnecessary. Its pattern is variable, ranging from mild focal spongiosis to a chronic spongiotic psoriasiform dermatitis with a mixed dermal inflammatory infiltrate and fungi in the cornified layer.[11] Routine histopathologic evaluation with hematoxylin-eosin staining may reveal cutaneous fungal elements, but periodic acidSchiff (PAS) staining is recommended to facilitate visualization. Hyphae may be detected in the stratum corneum of the epidermis. Infections with T rubrum or Trichophyton verrucosum may invade hairs and follicles. A mixed cellular inflammatory infiltrate is usually present in the papillary dermis, and neutrophils may extend into the horny layers above.

Medical Care
Most cases of tinea faciei are curable with topical antifungal agents. If a topical steroid has been applied, fungal folliculitis may be present.[16] Fungal folliculitis requires systemic therapy.

The frequency of daily application and duration of the treatment depend on the active ingredients of the preparation. Topical ciclopirox and terbinafine possess additional anti-inflammatory effects, which are especially important in the therapy for infections caused by zoophilic dermatophytes in which inflammatory reactions are usually prominent. Topical azoles are effective. Although rare, chronic and/or multiple lesions may require systemic therapy.

Medication Summary
Topical therapy may be sufficient if follicular papules are not present. The 2 classes of antifungal medication most commonly used to treat tinea faciei in practice are azoles and allylamines. Azoles inhibit lanosterol 14-alpha-demethylase, an enzyme that converts lanosterol to ergosterol, an important component of the fungal cell wall. Membrane damage leads to permeability problems and renders the fungus unable to reproduce. Allylamines inhibit squalene epoxidase, an enzyme that converts squalene to ergosterol; this inhibition also leads to the accumulation of toxic levels of squalene in the cell and to cell death. Several antifungal products from both classes are available for topical and systemic administration.[17]

Re-evaluation of the tinea diagnosis is important if clinical improvement is not observed after 4 weeks of therapy.

Antifungal agents
Class Summary

With these agents, the mechanism of action may involve an alteration in cell membrane permeability, DNA or RNA synthesis, or intracellular levels of metabolites that are toxic to the fungal cell.
View full drug information Butenafine (Mentax)

Potent antifungal related to allylamines. Available as a 1% cream.

View full drug information Clotrimazole topical (Lotrimin, Mycelex)

Broad-spectrum antifungal agent that inhibits yeast and fungal growth by altering cell membrane permeability. Frequently prescribed for patients with tinea faciei. Available without a prescription as 1% cream, solution or spray, and lotion.
View full drug information Miconazole (Femizole-7, Micatin, Absorbine)

Damages fungal cell-wall membrane by inhibiting biosynthesis of ergosterol. Membrane permeability is increased; this effect causes nutrients to leak out. Available as 2% cream, solution or spray, lotion, and powder. Lotion is preferred for use in intertriginous areas. If cream is used, apply sparingly to avoid maceration effects.
View full drug information Econazole (Spectazole)

Effective in cutaneous infections. Interferes with RNA and protein synthesis and metabolism. Disrupts fungal cell wall permeability, causing fungal cell death.

View full drug information Oxiconazole (Oxistat)

Damages fungal cell-wall membrane by inhibiting biosynthesis of ergosterol. Membrane permeability is increased causing nutrients to leak out. Available as a 1% cream or lotion.
View full drug information Undecylenic acid & derivatives (Desenex, Cruex, Fungoid AF, Gordochom)

Nonprescription agent rarely used in the treatment of tinea faciei. Available in cream or solution or spray.
View full drug information Tolnaftate (Absorbine, Aftate, Breeze, Dr. Scholl's Athlete's Foot)

Nonprescription medication available in 1% cream, solution or spray, and powder.

Haloprogin (Halotex)

Agent for use in the treatment of superficial cutaneous infections. Available in 1% cream and solution or spray.
View full drug information Ciclopirox (Loprox)

Interferes with synthesis of RNA, DNA, and proteins by inhibiting transport within fungal cells. Available as a 1% cream and lotion for skin.
View full drug information Terbinafine (Lamisil, Daskil)

Member of allylamine family, fungicidal agents that inhibit ergosterol synthesis by means of squalene epoxidase. Result is a decreased ergosterol level and accumulation of squalene, which is toxic to fungal cells.
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. Best results are noted 2-3 wk after treatment.
View full drug information Fluconazole (Diflucan)

Fungistatic activity. Synthetic oral antifungal (ie, broad-spectrum bistriazole) that selectively inhibits fungal cytochrome P-450 and sterol C-14 alpha-demethylation. This inhibition prevents the conversion of lanosterol to ergosterol, thereby disrupting cellular membranes.
View full drug information Griseofulvin (Fulvicin P/G, Gris-PEG)

Fungistatic activity. Interferes with microtubule impairs fungal cell division. Binds to keratin precursor cells. Keratin is gradually replaced with noninfected tissue, which is highly resistant to fungal invasions.

Deterrence/Prevention

The isolation and treatment of infected pets is of great importance.

Prognosis

The prognosis for patients with tinea faciei is usually good. The lesions respond to topical and oral antifungal treatment within 4-6 weeks.

Patient Education

For excellent patient education resources, visit eMedicine's Skin, Hair, and Nails Center. Also, see eMedicine's patient education article Ringworm on Body.