Tinea Faciei

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.

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.

The zoophilic dermatophyte Trichophyton species of Arthroderma benhamiae, most commonly from pet guinea pigs, is linked with an inflammatory tinea faciei in children and adolescents, particularly in Germany[2] but elsewhere too.[3] It has also been described in China, possibly transmitted from a fox.[4]

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.[5, 6] Preexisting factors may include diabetes mellitus.[7]

In Asia, Trichophyton mentagrophytes and Trichophyton rubrum are common.[8, 9] In a survey from Guangdong, China, T mentagrophytes and M canis were most commonly linked with tinea faciei.[10] In contrast, in North America Trichophyton tonsurans is the main pathogen isolated.

Frequency

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.[5, 11, 12, 13] Tinea faciei was shown to represent approximately 19% of all superficial fungal infections in the pediatric population with dermatomycoses.[14] Consecutive cases diagnosed between 2008 and 2016 were studied retrospectively. In an 8-year period, 72 tinea faciei cases have been diagnosed in a Lisbon hospital, 37 male and 35 female, aged between 8 months and 86 years.[15] Almost 60% were younger than 12 years.

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.[16]

Age

Tinea faciei may appear in persons of any age, with two peaks of disease incidence. Tinea faciei is extremely rare in neonates, with only a few cases described.[17] It has been described in a 14-day-old girl.[18] 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[19, 20, 21] ; these patients may acquire the infection from siblings or contact with pets. The other peak occurs in those aged 20-40 years. It has been described in a preterm infant due to Trichophyton rubrum, probably from skin-to-skin contact with the mother.[22]

The prognosis for patients with tinea faciei is usually good. The lesions respond to topical and oral antifungal treatment within 4-6 weeks. Scarring may occur in patients with Trichophyton schoenleinii infection; this is extremely rare.

For patient education resources, visit the Skin Conditions and Beauty Center. Also, see the patient education article Ringworm on Body.

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.[23, 24]

Tinea faciei, labeled as “mask tinea” since possibly potentiated by prolonged mask usage during the coronavirus disease 2019 (COVID-19) pandemic, has been described.[25]

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.[26] 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. It may be periocular.[27] See the images below.

In as many as 70% of patients with tinea faciei, various other dermatoses are considered. Tinea faciei is the most frequently misdiagnosed entity among cutaneous fungal infections. The atypical clinical features and incognito presentations support the separation of this disease from tinea corporis.[28]  Occasionally, tinea faciei may simultaneously occur with other forms of dermatophyte infections, especially tinea capitis and tinea corporis.

Tinea faciei caused by anthropophilic fungi may be less inflammatory and produce larger facial patches, whereas zoophilic ones may have more inflammatory and have smaller patches.[29]

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. 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. After warming the slide for a short time, the specimen is examined with a light microscope. 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. 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 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.[23] Routine histopathologic evaluation with hematoxylin-eosin staining may reveal cutaneous fungal elements, but periodic acid–Schiff (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.

Most cases of tinea faciei are curable with topical antifungal agents. If a topical steroid has been applied, fungal folliculitis may be present.[37] 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. Isoconazole nitrate and diflucortolone valerate combination therapy has been used successfully.[38]

Although rare, chronic and/or multiple lesions may require systemic therapy.

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

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.[39]

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

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.

Butenafine (Mentax)

Butenafine is a potent antifungal related to allylamines. It is available as a 1% cream.

Clotrimazole topical (Lotrimin, Mycelex)

Clotrimazole is a broad-spectrum antifungal agent that inhibits yeast and fungal growth by altering cell membrane permeability. It is frequently prescribed for patients with tinea faciei. Clotrimazole is available without a prescription as 1% cream, solution or spray, and lotion.

Miconazole (Femizole-7, Micatin, Absorbine)

Miconazole damages the fungal cell-wall membrane by inhibiting biosynthesis of ergosterol. Membrane permeability is increased; this effect causes nutrients to leak out. It is 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.

Econazole topical (Ecoza)

Econazole is effective in cutaneous infections. It interferes with RNA and protein synthesis and metabolism. Econazole disrupts fungal cell wall permeability, causing fungal cell death.

Oxiconazole (Oxistat)

Oxiconazole damages the fungal cell-wall membrane by inhibiting biosynthesis of ergosterol. Membrane permeability is increased, causing nutrients to leak out. It is available as a 1% cream or lotion.

Undecylenic acid & derivatives (Desenex, Cruex, Fungoid AF, Gordochom)

Undecylenic acid and derivatives are nonprescription agents rarely used in the treatment of tinea faciei. The formulation is available in cream or solution or spray.

Tolnaftate (Absorbine, Aftate, Breeze, Dr. Scholl's Athlete's Foot)

Tolnaftate is a nonprescription medication available in 1% cream, solution or spray, and powder.

Ciclopirox (Loprox)

Ciclopirox interferes with the synthesis of RNA, DNA, and proteins by inhibiting transport within fungal cells. It is available as a 1% cream and lotion for skin.

Terbinafine (Lamisil, Daskil)

Terbinafine is a member of the allylamine family, fungicidal agents that inhibit ergosterol synthesis by means of squalene epoxidase. The result is a decreased ergosterol level and an accumulation of squalene, which is toxic to fungal cells.

Itraconazole (Sporanox)

Itraconazole has fungistatic activity. It is a synthetic triazole antifungal agent that slows fungal cell growth by inhibiting cytochrome P-450–dependent synthesis of ergosterol, a vital component of fungal cell membranes. Best results are noted 2-3 weeks after treatment.

Fluconazole (Diflucan)

Fluconazole has fungistatic activity. It is a 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.

Griseofulvin (Fulvicin P/G, Gris-PEG)

Griseofulvin has fungistatic activity. It interferes with the microtubule annd impairs fungal cell division. Griseofulvin binds to keratin precursor cells. Keratin is gradually replaced with noninfected tissue, which is highly resistant to fungal invasions.