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Tinea faciei is a superficial dermatophyte infection limited to the glabrous skin of the face. 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.
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.
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.
Scarring may occur in patients with Trichophyton schoenleinii infection; this is extremely rare.
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.
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.
o The atypical clinical features and incognito presentations support the separation of this disease from tinea corporis.History Tinea faciei is frequently acquired from pets in the home. chin. vesicles. See the images below. similar to those of tinea corporis. and/or crusts. periorbital area. tinea faciei may simultaneously occur with other forms of dermatophyte infections. but it can also be spread from individuals with dermatophyte infection elsewhere on the body. Typical signs of dermatophyte infection of the glabrous skin. delayed or missed diagnosis may result. Erythematous scaling lesion on the cheek. o Occasionally. Some patients may have multiple lesions present in different areas of the face. followed by the nose. Multiple lesions on the face caused by Microsporum canis infection in a patient who also has tinea capitis. The most common locations are the cheeks. such as cutaneous lupus erythematosus. various other dermatoses are considered. atypical features are more frequently found on the glabrous skin than the typical patches of tinea corporis. especially tinea capitis and tinea corporis. o Tinea faciei is the most frequently misdiagnosed entity among cutaneous fungal infections. 12] Physical Because of the complex anatomy of the face. Tinea faciei may resemble other dermatoses. and allergic contact dermatitis. and forehead. polymorphous light eruption.[11. These signs include annular or serpiginous erythematous scaling patches with an active border composed of papules. Single or multiple erythematous patches without annular structure often resemble other dermatoses. In as many as 70% of patients with tinea faciei. Lesions are almost always pruritic. . may be present.
It includes direct microscopic examination for hyphal elements and culturing. Mycologic investigation is essential in the diagnosis of tinea faciei. . such as chlorazol black E. especially Microsporum canis. The collection of the surface scrapings is important for laboratory studies. Allergic Contact Dermatitis. Differentials Candidiasis. o After warming the slide for a short time. Culturing allows the identification of the causative pathogen. 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.[14. o Scrapings are placed in 10-20% potassium hydroxide (KOH) solution. 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. Acute Lupus Erythematosus. animal reservoirs of zoophilic dermatophytes. o Some authors suggest detection is enhanced with special stains. the specimen is examined with a light microscope. or Swartz-Lamkin stain.[13. in North America Trichophyton tonsurans is the main pathogen isolated. Bullous Lupus Erythematosus. as many as 30% of culture results may be negative. Trichophyton mentagrophytes and Trichophyton rubrum are common. Direct microscopic examination is the easiest mycologic procedure.Causes The causative agents of tinea faciei vary according to geographic regions. 2] In Asia. 15] In contrast. Cutaneous Contact Dermatitis. Parker blue-black ink. are global among pets and livestock. particularly in chronic infections. The latter helps to dissolve background keratinocytes to enable visualization of the fungal elements. usually with the addition of dimethyl sulfoxide (DMSO). Generally. Irritant Granuloma Annulare Lupus Erythematosus.
The 2 classes of antifungal medication most commonly used to treat tinea faciei in practice are azoles and allylamines. This media contains a color indicator that changes from yellow to red with the growth of dermatophytes after a few days of incubation. Topical azoles are effective. Although rare. o Histologic Findings Histologic examination may occasionally be useful for establishing the diagnosis. which are especially important in the therapy for infections caused by zoophilic dermatophytes in which inflammatory reactions are usually prominent. Routine histopathologic evaluation with hematoxylin-eosin staining may reveal cutaneous fungal elements. Several antifungal products from both classes are available for topical and systemic administration. Culturing is performed routinely with Sabouraud agar and the addition of cycloheximide and chloramphenicol. Hyphae may be detected in the stratum corneum of the epidermis. but periodic acid–Schiff (PAS) staining is recommended to facilitate visualization. Topical ciclopirox and terbinafine possess additional anti-inflammatory effects. If a topical steroid has been applied. Azoles inhibit lanosterol 14-alpha-demethylase. These substances inhibit the growth of bacteria and other contaminants. Fungal folliculitis requires systemic therapy. Medical Care Most cases of tinea faciei are curable with topical antifungal agents. chronic and/or multiple lesions may require systemic therapy. A mixed cellular inflammatory infiltrate is usually present in the papillary dermis. and neutrophils may extend into the horny layers above. Infections with T rubrum or Trichophyton verrucosum may invade hairs and follicles. . Its pattern is variable. this inhibition also leads to the accumulation of toxic levels of squalene in the cell and to cell death. o After 3-4 weeks of incubation. but it is usually unnecessary. an enzyme that converts lanosterol to ergosterol. an important component of the fungal cell wall. The frequency of daily application and duration of the treatment depend on the active ingredients of the preparation. Medication Summary Topical therapy may be sufficient if follicular papules are not present. Membrane damage leads to permeability problems and renders the fungus unable to reproduce. Dermatophytes may be diagnosed by using special media for rapid detection. the final identification is based on morphologic and microscopic findings in the colonies. an enzyme that converts squalene to ergosterol. ranging from mild focal spongiosis to a chronic spongiotic psoriasiform dermatitis with a mixed dermal inflammatory infiltrate and fungi in the cornified layer. fungal folliculitis may be present. Allylamines inhibit squalene epoxidase.
View full drug information Econazole (Spectazole) Effective in cutaneous infections. or intracellular levels of metabolites that are toxic to the fungal cell. Frequently prescribed for patients with tinea faciei. Disrupts fungal cell wall permeability. Available without a prescription as 1% cream. apply sparingly to avoid maceration effects. Available as a 1% cream. Membrane permeability is increased. causing fungal cell death. solution or spray. Interferes with RNA and protein synthesis and metabolism. Micatin. the mechanism of action may involve an alteration in cell membrane permeability. this effect causes nutrients to leak out. and lotion. Absorbine) Damages fungal cell-wall membrane by inhibiting biosynthesis of ergosterol. Antifungal agents Class Summary With these agents. View full drug information Clotrimazole topical (Lotrimin. solution or spray. DNA or RNA synthesis. lotion. View full drug information Butenafine (Mentax) Potent antifungal related to allylamines. Mycelex) Broad-spectrum antifungal agent that inhibits yeast and fungal growth by altering cell membrane permeability. . Available as 2% cream.Re-evaluation of the tinea diagnosis is important if clinical improvement is not observed after 4 weeks of therapy. Lotion is preferred for use in intertriginous areas. View full drug information Miconazole (Femizole-7. and powder. If cream is used.
Gordochom) Nonprescription agent rarely used in the treatment of tinea faciei.View full drug information Oxiconazole (Oxistat) Damages fungal cell-wall membrane by inhibiting biosynthesis of ergosterol. Cruex. View full drug information Tolnaftate (Absorbine. View full drug information Undecylenic acid & derivatives (Desenex. Dr. Breeze. DNA. Available as a 1% cream or lotion. Haloprogin (Halotex) Agent for use in the treatment of superficial cutaneous infections. Fungoid AF. and proteins by inhibiting transport within fungal cells. Scholl's Athlete's Foot) Nonprescription medication available in 1% cream. and powder. solution or spray. Available in 1% cream and solution or spray. Aftate. View full drug information Terbinafine (Lamisil. Available as a 1% cream and lotion for skin. View full drug information Ciclopirox (Loprox) Interferes with synthesis of RNA. Available in cream or solution or spray. Daskil) . Membrane permeability is increased causing nutrients to leak out.
. Keratin is gradually replaced with noninfected tissue. This inhibition prevents the conversion of lanosterol to ergosterol. see eMedicine's patient education article Ringworm on Body. fungicidal agents that inhibit ergosterol synthesis by means of squalene epoxidase. Binds to keratin precursor cells. The lesions respond to topical and oral antifungal treatment within 4-6 weeks. Hair. Patient Education For excellent patient education resources. Deterrence/Prevention The isolation and treatment of infected pets is of great importance. visit eMedicine's Skin. Synthetic oral antifungal (ie. which is toxic to fungal cells. Result is a decreased ergosterol level and accumulation of squalene. Prognosis The prognosis for patients with tinea faciei is usually good.Member of allylamine family. Also. Best results are noted 2-3 wk after treatment. View full drug information Itraconazole (Sporanox) Fungistatic activity. and Nails Center. broad-spectrum bistriazole) that selectively inhibits fungal cytochrome P-450 and sterol C-14 alpha-demethylation. which is highly resistant to fungal invasions. a vital component of fungal cell membranes. View full drug information Griseofulvin (Fulvicin P/G. thereby disrupting cellular membranes. Synthetic triazole antifungal agent that slows fungal cell growth by inhibiting cytochrome P-450–dependent synthesis of ergosterol. Gris-PEG) Fungistatic activity. View full drug information Fluconazole (Diflucan) Fungistatic activity. Interferes with microtubule impairs fungal cell division.
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