Tinea faciei

Etiology

• Fungal infection of the superficial skin.
• Caused by dermatophytes, which require keratin for growth.
  • Trichophyton tonsurans and T. rubrum, (harbored by humans) as well as Microsporum canis (harbored by animals) are the most common infectious species.
  • Worldwide, rates of tinea faciei due to T. interdigitale are increasing.
• Acquired by direct contact with infected humans or, less commonly, animals.
  • Can also be acquired indirectly by exposure to fomites or fungi-laden soil.

Epidemiology

• Tinea faciei accounts for approximately 4% of tinea corporis, a general term for tinea manifesting anywhere on the glabrous skin (Lin, 2004).
  • Tinea corporis is sometimes misleadingly called “ringworm,” despite the fact that it is a fungal infection. 
• Disease is most likely to present from early childhood to the fourth decade of life (Lin, 2004).
  • Young children are likely to acquire tinea faciei from facial contact with domesticated animals.
  • Tinea faciei has been reported in neonates as early as day 2 of life (Alkeswani, 2018).
  • Tinea infections account for nearly 30% of skin infections in high school athletes due to their contact with fungal-laden athletic equipment. One-fourth of these cases occur on the head or face (Ashack, 2016).
• Tinea faciei is the most commonly misdiagnosed cutaneous fungal infection and is particularly underdiagnosed in the periocular region (Basak, 2011 & Lin, 2004).
  • A retrospective study found that the majority of cases were not diagnosed until 1-4 months after symptom onset (Aste, 2009).
  • Misdiagnosis is due to its highly polymorphic and sometimes subtle presentation.
    • This is problematic as misdiagnosis leads to inappropriate treatment with corticosteroids, which can worsen disease, alter presentation and hinder diagnosis (see clinical presentation and management).
      • The term given to a fungal disease altered in appearance by an incorrect treatment (i.e. topical corticosteroids) is ‘tinea incognita.’
  • For the above reasons, it is difficult to determine the true incidence of tinea faciei.

Clinical features

• Classical presentation includes single or multiple annular lesions with central clearing and scale formation (Figure 1).
• It may be acute in onset with rapid extension or subacute/chronic with slow spread.
• There is often an erythematous, inflamed rim around the rash, known as the active border.
• A periocular rash accompanied by eyelash and/or eyebrow hair loss is highly specific for tinea faciei.
• Other presenting features include:
  • Periocular tenderness
  • Periocular edema
  • Pruritus and burning that is worse after sun exposure
  • Adenopathy
  • Lesion alteration with the use of topical steroids
    • Steroids reduce erythema and inflammation and may lead to changes in skin pigmentation, skin thinning and striae formation. This modified clinical appearance makes diagnosis more difficult.
• Atypical features are observed in approximately 40% of cases and include (Aste, 2009):
  • Confluent erythematous plaques
  • Vesicles and/or bullae
  • Papules and/or pustules
• Tinea faciei on the eyelid mimicking hordeolum has been reported (Yin, 2018).

Other diagnostic tests (often required for diagnosis)

• Microscopic examination of skin scrapings in 10% potassium hydroxide (KOH) solution
• Woods lamp examination
• Fungal culture (rarely used)
  • False negative rate of fungal culture is up to 30% (Lin, 2004).
• Histologic examination of tissue
  • Periodic acid–Schiff (PAS) staining is key to ruling out other dermatoses.
    • Hyphae in the stratum corneum is specific to tinea infection and seen with PAS staining.

• Eczema
• Impetigo
• Acne rosacea
• Seborrheic dermatitis
• Periorificial dermatitis
• Contact dermatitis
• Herpes simplex virus
• Actinic keratoses
• Cutaneous lupus erythematosus
• Granuloma annulare
• Cutaneous leprosy
• Erythema annulare centrifugum
• Erythema migrans

• Medical therapy:
• Topical antifungal cream is first line for tinea faciei.
• Commonly used regimens are topical azoles (i.e. ketoconazole) for 4 weeks or topical allylamines (i.e. terbinafine) for 1 week.
• Oral griseofulvin for 8 weeks or oral terbinafine for 4 weeks may be used if disease is non-responsive to topical treatment.
• If disease infiltrates past the superficial cutaneous layers (i.e. into the vellus hair follicles of the face), oral antifungal treatment is often required.
• Long duration of treatment (weeks to months) is required to ensure complete eradication of fungi.
• In some cases, oral and topical antifungals are used in combination.
• Corticosteroids are contraindicated as they do not eradicate fungi from the skin surface and are associated with:
• Recurrence
• Spread of disease 
• Antifungal resistance
• Surgical therapy: none
• Prognosis: complete resolution with hair restoration takes approximately 3 months with appropriate treatment.   

• Inadequate eradication of infection leading to chronic recurrence.
• In rare cases, the initial infection site can be asymptomatic, leading to chronic infection at another site(s).
• A child with a decade of recurrent tinea faciei involving the eyelid was found to be an asymptomatic carrier of tinea capitis, with repeated autoinoculation of the face (Kawachi, 2010)
• Scarring
• Kerion (formation of a fungal abscess) 
• Adverse effects of treatment:
• Griseofulvin
• Nausea
• Vomiting
• Photosensitivity
• Terbinafine
• Liver toxicity


Photograph courtesy of D@nderm Atlas of Clinical Dermatology.

Figure 1. Periocular tinea faciei due to infection with Trichophyton mentagrophytes. An erythematous annular rash with central clearing and edema of the upper eyelid can be seen.

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