Dermatophyte infections

Dermatophyte infections (tinea) are caused by keratinophilic fungi, most commonly of the Trichophyton, Microsporum, and Epidermophyton genera, and affect the skin, hair, and nails. Depending on the site of infection, the clinical manifestations, differential diagnoses, and management may differ. In general, clinical features include well-defined lesion(s) with pruritus, scaling, and erythema. Visual inspection may be adequate for diagnosing dermatophyte infections involving the skin (e.g., tinea pedis, tinea corporis, and tinea cruris), for which topical treatment is usually sufficient. If the diagnosis remains uncertain or if systemic therapy is likely needed (e.g., for suspected tinea capitis or tinea unguium), additional testing is necessary to confirm the diagnosis, e.g., KOH test or fungal culture. Systemic antifungal therapy is usually required for weeks to months, and patients require monitoring for potential adverse effects of therapy. Reinfection is common; screen and treat close contacts and advise patients on infection prevention measures (e.g., not sharing towels and keeping skin clean, cool, and dry).

Tinea versicolor, despite its name, is not caused by dermatophytes and is discussed in another article.

Causative pathogens ^[1][2]

• Dermatophytes are fungi that infect keratinized tissue and belong to the Trichophyton (most common), Microsporum, and Epidermophyton genera.
• The most common causative pathogen of dermatophyte infection is Trichophyton rubrum.

Risk factors ^[1][2]

• Risk factors common to all dermatophyte infections include:
  • Diabetes mellitus
  • Immunodeficiency (e.g., HIV, trisomy 21)
  • Poor circulation, peripheral arterial disease
  • Maceration of skin (e.g., due to excessive sweating)
• Additional risk factors specific to the site of infection are detailed in the relevant sections.

Transmission ^[1]

• Indirect contact with fomites (e.g., combs, towels, shoes)
• Direct skin-to-skin transmission with infected individuals or animals

• Features vary based on site of infection; see relevant sections under “Subtypes and variants” for details. ^[1][2]
• In general, clinical features include well-defined lesion(s) with pruritus, scaling, and erythema.
• Lesions may be accompanied by an id reaction (a type of hypersensitivity reaction); manifestations include: ^[1]
  • Widespread pruritic lesions (papular, vesicular, or eczematous)
  • Often located at sites distant from the fungal infection
  • Can occur after initiation of therapy
• Rare features include:
  • Majocchi granuloma ^[1][3]
    • Rare granulomatous dermal reaction to fungal infection of hair follicle and surrounding tissue
    • Manifestations are variable and include perifollicular pustules, nodules, or papules within an erythematous plaque.
    • May develop after tinea corporis is treated with topical corticosteroids
  • Tinea incognito ^[1][4]
    • Dermatophyte infection with an atypical presentation (e.g., no scaling at the border of lesions, reduced erythema)
    • May occur in patients with immunosuppression or after using topical steroids ^[1][2][4]

Worsening of symptoms of an undifferentiated cutaneous lesion following empiric treatment with topical steroids suggests a dermatophyte infection. ^[2]

See also relevant sections under “Subtypes and variants” for differential diagnoses specific to the site of involvement.

• Impetigo
• Dermatitides (e.g., seborrheic dermatitis, atopic dermatitis, contact dermatitis)
• Tinea versicolor
• Herald patch (pityriasis rosea)
• Cutaneous candidiasis
• Erythrasma
• Psoriasis
• Intertrigo
• Nummular eczema
• Erythema multiforme
• Granuloma annulare

The differential diagnoses listed here are not exhaustive.

Diagnosis ^[2][5]

• Tinea corporis, tinea cruris, and tinea pedis are usually diagnosed clinically.
• Indications for diagnostic testing
  • Diagnostic uncertainty
  • Patients requiring systemic therapy (e.g., tinea capitis, tinea unguium, severe or refractory infection)
• Diagnostic tests
  • KOH test: branching segmented hyphae, spores ^[2][5]
  • Fungal culture: high accuracy but results take 2–6 weeks ^[2]
  • Wood lamp examination ^[1][2]
    • Used as an adjunct to KOH or fungal culture for suspected Microsporum spp.
    • Findings ^[6]
      • Blue-green fluorescence of Microsporum spp.
      • Trichophyton tonsurans does not fluoresce.
    • False negatives may occur if the patient has recently bathed.
  • Skin biopsy or nail biopsy : higher sensitivity when used in combination with KOH and/or fungal testing

For patients with widespread dermatophyte infection, consider working up for underlying immunosuppression, e.g., HIV testing.

Treatment ^[1][2]

• Start antifungal therapy.
• Optimize management of any concurrent immunosuppression.
• Reassess after 2–4 weeks to determine response. ^[1]
• Monitor patients on systemic therapy for potential adverse effects.
• See specific sections for further information.

Because dermatophytes are resistant to nystatin, it should not be used for the treatment of dermatophyte infections. ^[2][7]

Topical antifungal therapy for dermatophyte infections ^[1][2][8]

Indications

• Tinea pedis
• Tinea corporis
• Tinea cruris
• Tinea unguium in children
• Adjunct to systemic therapy in tinea capitis
• Alternative to systemic therapy in patients who prefer or require topical treatment

Agents

• Azoles (e.g., miconazole; , clotrimazole ) ^[1]
• Tolnaftate ^[1]
• Ciclopirox ^[1]
• Terbinafine ^[1]

For topical therapy, calculate the finger-tip unit to prescribe a quantity sufficient for the treatment duration. ^[9]

Systemic antifungal therapy for dermatophyte infections ^[1][2][8]

Indications

• Tinea capitis
• Tinea barbae
• Tinea unguium in adults
• Unsuccessful topical treatment (refractory disease)
• Extensive spread (e.g., in patients with immunodeficiency)
• Majocchi granuloma ^[3]

Agents

• Terbinafine granules or tablets (off-label) ^[1][2]
• Griseofulvin suspension (off-label) or tablets (off-label) ^[1][2][10]
• Fluconazole (off-label) ^[1][2][10]

Griseofulvin is teratogenic and associated with a risk of chromosomal abnormalities. It is contraindicated in pregnancy, and both male and female individuals should use contraception for 6 months after stopping griseofulvin. ^[10]

Oral ketoconazole is not recommended for treating dermatophyte infections due to the risk of severe side effects, including hepatotoxicity and adrenal insufficiency. ^[2]

Laboratory monitoring ^[2]

Monitor patients on systemic antifungal therapy for adverse effects, which can be serious and include hepatotoxicity.

• Baseline studies
  • Not routinely required before initiating treatment with griseofulvin
  • Obtain baseline CBC and liver chemistries before initiating treatment with other systemic antifungals.
  • Obtain serum creatinine levels before initiating treatment with fluconazole.
• Serial monitoring
  • All patients: Monitor CBC and liver chemistries every 4–8 weeks while on systemic antifungal therapy.
  • Patients taking griseofulvin: Monitor serum creatinine levels every 8 weeks.

Infection control measures ^[1][2]

Advise all patients on measures to prevent transmission of dermatophyte infections or reinfection. See also relevant sections for measures specific to the site of infection.

• Identify and treat dermatophyte infections in other areas.
• Advise patients not to share items that could spread infection (e.g., shoes, towels, combs, hats).
• Use a separate towel to dry infected areas.
• Examine and treat close household contacts; advise veterinary assessment and treatment of pets.
• Transmission precautions are usually no longer required once patients start treatment.

The clinical presentation, differential diagnoses, and management of dermatophyte infections vary by site of infection.

Tinea capitis is a dermatophyte infection of the hair of the scalp. It mainly occurs in prepubertal children but can affect individuals at any age. ^[1]

Pathogens ^[1]

• Most commonly caused by T. tonsurans
• Microsporum canis and Microsporum audouinii (zoonotic transmission) account for < 5% of cases in the United States. ^[1]

Clinical features ^[1][2]

• Round, pruritic scaly plaques with broken hair shafts (black dot pattern) or loss of hair (gray patch pattern) in affected areas
• Regional lymphadenopathy (postauricular, suboccipital, cervical) may be present.
• Severe manifestations include:
  • Kerion: characterized by a deep, boggy plaque with pustules
  • Tinea favus: characterized by scarring alopecia and crusting; caused by chronic infection with Trichophyton schoenleinii

Management

Diagnosis ^[1][2]

• Diagnostic tests (e.g., KOH test, fungal culture) are indicated for all patients.
• Dermoscopy can show comma, corkscrew, and zigzag hairs. ^[1][11][12]

False-negative rates in fungal cultures of kerion are high; consider sampling any concurrent noninflammatory lesions of tinea capitis to improve sensitivity. ^[2][13]

T. tonsurans does not produce fluorescence under Wood lamp. ^[6][10]

Treatment ^[1][2][10]

• All patients: Initiate systemic antifungal therapy for dermatophyte infections.
  • Therapy may be initiated empirically while awaiting culture results.
  • Treat for ≥ 6 weeks; continue treatment for 2 weeks after symptoms resolve. ^[1][2][10]
• Patients with kerion ^[1]
  • Prompt treatment with systemic griseofulvin is recommended. ^[2]
  • Wet compresses can be used to soften and remove crusts.
  • Consider antibiotics if secondary bacterial infection is confirmed; see “Antibiotic therapy for skin and soft tissue infections.”
  • Some experts suggest systemic corticosteroid therapy for severe cases to minimize the risk of scarring alopecia.

Griseofulvin is preferred for patients with tinea capitis due to Microsporum spp. infection and those with kerion. When available, terbinafine is preferred for the treatment of tinea capitis due to Trichophyton spp. ^[2][10]

Prevention of transmission ^[1][2][10]

• Prescribe topical antifungal shampoo (e.g., selenium sulfide or ketoconazole ) for:
  • Infected individuals: as adjunctive therapy for 2 weeks to reduce transmission ^[1][2]
  • Asymptomatic close contacts: 2–4 weeks to prevent infection ^[2][10]
• Disinfect or replace items that have been in contact with the patient's head.
• Recommend evaluation and treatment of any pets.
• See also “Infection control measures for dermatophyte infections.”

Children receiving treatment do not need to be removed from school or daycare. ^[1]

Differential diagnoses ^[1][2]

• Dermatitides (e.g., seborrheic dermatitis, atopic dermatitis, contact dermatitis)
• Alopecia areata
• Trichotillomania
• Lice infestation
• Discoid lupus
• See also “Differential diagnoses of dermatophyte infections.”

Broken hair shafts within a scaly lesion and associated posterior cervical lymphadenopathy are characteristic features of tinea capitis and can help distinguish it from common differential diagnoses. ^[1][2]

Prognosis

• Hair usually regrows completely.
• Protracted infection and kerion may result in permanent scarring alopecia. ^[1]

Tinea barbae is a rare dermatophyte infection affecting the hair of the beard. Individuals working with animals are at increased risk. ^[14][15][16]

Pathogens ^[14][15][16]

• Most commonly T. verrucosum and T. mentagrophytes (zoonotic transmission)
• Less commonly, T. rubrum causes tinea barbae.

Clinical features ^[15]

• Erythematous papules, patches, and pustules, and crusting around the hair (kerion-like plaques)
• Loss of hair within the lesions
• Lymphadenopathy may be present if there is long-standing or secondary infection.

Management

• Diagnosis: Confirmatory studies and/or dermatoscopy are recommended. ^[16]
• Treatment: systemic antifungal therapy; same as for tinea capitis ^[15]
• See also “Management of dermatophyte infections.”

Differential diagnoses ^[15]

• Bacterial folliculitis
• Perioral dermatitis
• Pseudofolliculitis barbae
• Contact dermatitis
• Herpes simplex
• Acne vulgaris
• Rosacea
• See also “Differential diagnoses of dermatophyte infections.”

Tinea corporis is a dermatophyte infection of the skin of the face, torso, and limbs (excluding hands and feet).

Pathogens ^[1][17]

• Most commonly caused by T. rubrum
• More recently, the number of infections caused by T. indotineae is increasing.

Clinical features ^[1]

• Round, pruritic, initially erythematous plaque(s)
• Develops into a round pruritic plaque with central clearing and a scaling, raised border (ringworm appearance)

Management ^[1][2]

• Diagnosis is usually clinical.
• Treatment
  • Mild and moderate infections
    • Start topical antifungal therapy for dermatophyte infections.
    • Continue therapy for 2–4 weeks after symptoms resolve. ^[1]
  • Refractory and/or severe infections
    • Start systemic antifungal therapy for dermatophyte infections.
    • Continue therapy for 1–3 months ^[18]
• See also “Management of dermatophyte infections” for details; on infection control measures, monitoring, and follow-up.

Do not use combination antifungal and topical steroid creams because combination creams are less effective and can lead to Majocchi granuloma. ^[1]

Differential diagnoses ^[1][2]

See “Differential diagnoses of dermatophyte infections.”

Tinea cruris (jock itch) is a dermatophyte infection of the inguinal, genital, and/or perianal area.

Etiology ^[1]

• Pathogens: most commonly T. rubrum, T. mentagrophytes, and Epidermophyton floccosum
• Risk factors include:
  • Male sex
  • Obesity
  • Tight-fitting clothes
  • Noncotton underwear
  • Tinea pedis or tinea unguium
  • See also “Risk factors common to all dermatophyte infections.”

Clinical features ^[1]

• Pruritic erythematous or hyperpigmented plaques that spread centrifugally
• Similar to tinea corporis but often without central clearing
• Scaling, raised border
• Spares the scrotum ^[1][2]

Management ^[1]

• Diagnosis is usually clinical.
• Treatment is the same as for tinea corporis.
• Measures to prevent reinfection
  • Concurrent treatment of tinea pedis and tinea unguium
  • Wearing loose-fitting clothing
• Measures to prevent spread of infection
  • To others: Avoid sharing of towels.
  • Autoinoculation: Advise patients to dry the groin area before the feet.
• See also “Management of dermatophyte infections.”

Differential diagnoses ^[1][2]

See “Differential diagnoses of dermatophyte infections.”

Tinea pedis (athelete's foot) is a dermatophyte infection of the foot and is the most common type of dermatophyte infection. ^[1][19]

Etiology

• Pathogens: most commonly T. rubrum, T. mentagrophytes, T. interdigitale, and E. floccosum ^[1][17]
• Risk factors ^[1]
  • Occlusive, tight footwear
  • Use of public showers, swimming pools, and locker areas
  • See also “Risk factors common to all dermatophyte infections.”

Clinical features ^[1]

• Interdigital (most common): chronic, pruritic, erythematous scaling and erosions between the toes and/or fingers
• Moccasin: confluent hyperkeratotic thickening of the skin on soles of feet
• Vesicular: pruritic or painful vesicular lesions and erythema, often on the medial foot
• May be accompanied by tinea unguium, tinea manuum, or tinea cruris
• May be complicated by secondary bacterial superinfection (e.g., erysipelas)

Management ^[1][2]

• Diagnosis is usually clinical.
• Treatment ^[1][2]
  • Mild infection: Start topical antifungal therapy for dermatophyte infections.
  • Severe or refractory infection: Start systemic antifungal therapy for dermatophyte infections.
  • Duration: 2 weeks for mild infections; longer for severe infections ^[1]
• Advise patients to avoid swimming pools, locker rooms, and showers until treatment has been completed.
• Prevention of reinfection: Advise patients on the following measures. ^[1]
  • Drying between each toe
  • Foot powders and antifungal treatment of shoes
  • Open shoes in warm, humid weather
  • Breathable socks
  • Footwear for public showers, locker rooms, and swimming pools
• See also “Management of dermatophyte infections.”

Differential diagnoses ^[1][2]

• See “Differential diagnoses of dermatophyte infections.”
• Additional conditions to consider for patients with tinea pedis include:
  • Dyshidrotic eczema
  • Juvenile plantar dermatosis
  • Palmoplantar keratoderma

Tinea manuum is a dermatophyte infection of the hand. ^[20][21]

Pathogens ^[20][21]

Most commonly T. rubrum, T. mentagrophytes, and E. floccosum

Clinical features ^[21]

• Vesicles or scaling affecting the palms or dorsum of the hand
• Pruritus
• Rarely seen in isolation; the majority (> 80%) of individuals with tinea manuum also have tinea pedis.
• Two feet-one hand syndrome: Both feet and a single (usually the dominant) hand are affected.

Management ^[21]

• Diagnosis: usually clinical; confirmatory studies are indicated in case of diagnostic uncertainty.
• Treatment: Systemic antifungal therapy is usually required as infection typically affects multiple sites.
  • Systemic antifungals for 2–4 weeks, options include:
    • Terbinafine (off-label) ^[21]
    • Itraconazole (off-label) ^[21]
  • May be used in combination with topical agents for 2 weeks, options include:
    • Luliconazole ^[21]
    • Naftifine ^[21]
• See also “Management of dermatophyte infections.”

Differential diagnoses ^[21]

• See “Differential diagnoses of dermatophyte infections.”
• Additional conditions to consider for patients with tinea manuum include:
  • Dyshidrotic eczema
  • Palmoplantar pustulosis

Tinea unguium is a dermatophyte infection of the nail and is the most common cause of onychomycosis.

Etiology

• Most commonly T. rubrum, T. mentagrophytes, and E. floccosum ^[1][22]
• Risk factors ^[1][8]
  • Age > 60 years
  • Repeated nail injury
  • Chronic use of tobacco
  • Peripheral vascular disease
  • See also “Risk factors common to all dermatophyte infections”

Clinical features ^[1][8]

• Discolored (white, gray, or yellow), thickened, distorted, and brittle nails
• Left untreated, nail structure may be completely lost. ^[22]
• May be associated with tinea pedis and/or tinea manuum

Diagnosis ^[1][8]

• Diagnostic confirmation is recommended before initiating treatment.
• Any or all of the following studies can be used to confirm the diagnosis.
  • KOH test
  • Fungal culture with or without PAS staining
  • NAAT of nail clippings or subungual debris

Treatment ^[1][8]

• Tinea unguium may be treated with systemic and/or topical therapy.
• Treatment efficacy may be improved by:
  • Frequent nail trimming and debridement ^[1][8]
  • Combining topical treatment with laser therapy ^[8]
• Toenail removal is recommended for refractory or severe infection. ^[8]

Topical therapy

• Indications ^[1][8]
  • Pediatric patients
  • Infections that do not involve the nail matrix
  • Prophylaxis against recurrence
• Options
  • Efinaconazole ^[1][8]
  • Tavaborole ^[1][8]
  • Ciclopirox lacquer ^[1][8]
• Duration of therapy: 24 weeks for fingernails; 48 weeks for toenails ^[8]

Systemic therapy

Obtain baseline laboratory studies before initiating treatment and monitor patients for adverse effects. See “Monitoring patients taking systemic antifungal therapy.”

• Most effective agents
  • Terbinafine tablets (off-label in children) ^[1][8]
  • Itraconazole (off-label in children)
    • Toenail infections (continuous dosing) ^{[1][8][23][24]}
    • Fingernail infections (pulsed dosing) ^{[1][8][23][24]}
• Duration of therapy
  • Until the entire nail grows out
  • Typically 6 weeks for fingernails and 12 weeks for toenails ^[1][8]

Systemic antifungal therapy is more effective than topical therapy but requires monitoring for potential adverse effects.

Prevention of reinfection ^[1][8]

• Disinfecting shoes and socks
• Keeping toenails short and feet cool and dry
• Early treatment of tinea pedis
• Consider prophylactic treatment with a topical antifungal twice a week for recurrent infections.
• See also “Infection control measures for dermatophyte infections.”

Differential diagnoses ^[2][8]

• Recurrent nail trauma
• Paronychia
• Herpetic whitlow
• Noninfective onycholysis
• Psoriasis
• Lichen planus