Tinea Barbae

Both conditions are dermatophyte infections of hair bearing skin in which the fungus reaches the hair follicle. They differ in site and mechanism. Tinea barbae is infection of the beard and moustache area of adult men. Majocchi granuloma is a granulomatous infection of the follicle and surrounding dermis that follows rupture of an infected follicle, and it can occur at any hair bearing site.

The common clinical principle is that dermatophytes in the hair follicle are out of reach of topical therapy. Both diagnoses therefore need oral treatment.

Epidemiology and organisms

Tinea barbae affects adult men with terminal beard hair. It is rare in women, in children and before puberty. It is uncommon in urban populations and most frequent in farming communities, where contact with cattle and horses is usual.

Transmission occurs through animal contact, contaminated razors, brushes and barbershop equipment, and autoinoculation from tinea pedis, cruris or capitis. Shaving damages follicles and spreads the organism along the beard. Topical corticosteroids applied to a presumed bacterial or eczematous rash are a common precipitant.

Pathogenesis

The hair infection is ectothrix. Large spored arthroconidia (5 to 8 micrometres) cover the surface of the shaft, and hyphae enter the follicle. Zoophilic species provoke a marked delayed type hypersensitivity reaction with neutrophilic and granulomatous inflammation of the follicle. Anthropophilic species provoke little reaction.

Clinical patterns

• Deep inflammatory (kerion like) form: boggy, tender, erythematous nodules and plaques studded with pustules, discharging pus from follicles. Hairs are loose and pull out painlessly. Crusting and matting of the beard develop, with regional lymphadenopathy, fever and malaise in severe disease. Untreated disease leaves scarring and permanent hair loss.
• Superficial (sycosiform) form: erythematous, scaly or crusted patches with follicular papules and pustules, and broken hairs, resembling bacterial sycosis. Inflammation is mild, and the course is chronic.
• Annular form: ringworm like plaques on the beard area with an active scaly edge.

The upper lip, chin and submandibular region are the usual sites. Involvement is often unilateral.

Differential diagnosis

Laboratory diagnosis

• Specimen: plucked hairs with roots, pus expressed from follicles, and crusts. Epilation of loosened hairs is painless in the inflammatory form.
• Potassium hydroxide preparation: large spored ectothrix arthroconidia around the hair shaft, with hyphae within the shaft. In the Trichophyton rubrum form, hyphae and arthroconidia are seen with endothrix tendencies.
• Culture: Sabouraud dextrose agar with chloramphenicol, with and without cycloheximide, at 25 to 30 degrees Celsius for 3 to 4 weeks. Trichophyton verrucosum is slow growing, and needs thiamine and sometimes inositol with incubation at 37 degrees Celsius.
• Bacterial culture: taken in parallel, because secondary bacterial infection is frequent.
• Histopathology: rarely needed, shows perifollicular and follicular neutrophilic and granulomatous inflammation, with hyphae and arthroconidia in hair shafts on periodic acid Schiff.

Treatment

Topical therapy alone is inadequate. Oral therapy is continued until the lesions clear, which usually takes several weeks.

Supportive measures:

• Warm saline or aluminium acetate compresses for crusting, and gentle removal of crusts and loose hairs.
• Antibacterial therapy only for confirmed bacterial superinfection.
• Incision and drainage are avoided, because the inflammation is a hypersensitivity response and not an abscess.
• A short course of oral prednisolone (0.5 to 1 mg per kg daily for 1 to 2 weeks) may be used in severe, painful inflammatory disease, with an effective oral antifungal. Benefit is not established.
• Stop shaving with shared razors during treatment, and discard or disinfect razors and brushes.
• Treat tinea pedis, cruris and capitis in the same patient.
• Examine and treat infected animals and household contacts.

Terbinafine resistant isolates are treated with itraconazole 200 mg daily for at least 4 weeks, with sequencing and susceptibility work where available.

Definition and epidemiology

Majocchi granuloma (dermatophytic granuloma, nodular granulomatous perifolliculitis) is a deep dermatophyte infection in which fungal hyphae and arthroconidia penetrate the follicular wall and invade the perifollicular dermis, provoking a granulomatous reaction. It is a deeper process than ordinary tinea corporis.

Trichophyton rubrum is the commonest cause by far. Trichophyton mentagrophytes, Trichophyton tonsurans, Trichophyton verrucosum, Microsporum canis and Nannizzia gypsea are less frequent causes. The organism is a keratinophilic dermatophyte that has entered living tissue through the follicle.

Two clinical settings are recognised:

Risk factors

• Shaving, waxing and plucking of legs and other sites, which injure follicles and spread organisms.
• Topical corticosteroids, including combined steroid antifungal creams, used on undiagnosed tinea.
• Occlusive dressings and occlusive clothing, and trauma.
• Pre existing tinea pedis, onychomycosis or tinea cruris, which provide the source.
• Systemic immunosuppression.
• Inherited defects of antifungal immunity, especially CARD9 deficiency, in which deep dermatophytosis is extensive and recurrent.

Pathogenesis

Hairs shaved or plucked leave a damaged follicle. Dermatophyte arthroconidia and hyphae in the hair penetrate the follicle wall.

In the healthy host, the follicle ruptures and fungal elements enter the dermis, where neutrophils, macrophages and multinucleate giant cells form a granuloma around the hair remnant and the organism. Topical corticosteroids suppress the surface response and promote fungal persistence and extension.

In the immunosuppressed host, the fungus spreads deeper and more widely through the dermis and subcutis, and, in CARD9 deficiency, to lymph nodes and viscera.

Clinical features

• Follicular papules and pustules, erythematous or violaceous, on the legs, forearms, face or scalp, and sometimes in groups or in an annular arrangement.
• Larger inflammatory nodules, plaques with a verrucous or boggy surface, and in the deep form, subcutaneous nodules, abscesses and draining sinuses.
• Mild itch, tenderness or no symptoms.
• Evidence of tinea elsewhere, particularly tinea pedis or onychomycosis.
• Tinea incognito at the surface, after topical corticosteroid use.
• Systemic features are unusual except in the immunosuppressed host with extensive disease.

Differential diagnosis

Laboratory diagnosis

• Specimens: biopsy (punch or excision), pus from sinuses, plucked hairs with follicles, and scale. Scrapings of the surface often show no fungus, because the organisms are in the follicle and the dermis.
• Potassium hydroxide preparation of plucked hairs and follicular contents: hyphae and arthroconidia in the hair shaft or the follicular material.
• Culture of tissue or hair: the biopsy sample is minced and not ground. It is placed on Sabouraud dextrose agar with chloramphenicol, with and without cycloheximide. Culture identifies the dermatophyte and permits susceptibility testing.
• Histopathology: perifollicular and dermal granulomatous inflammation with neutrophils, lymphocytes, histiocytes and multinucleate giant cells, rupture of the follicular wall, and hyphae and spores in the follicle, hair shaft and dermis on periodic acid Schiff or Grocott methenamine silver. Fungal elements may be sparse, so serial sections are examined.
• Polymerase chain reaction and sequencing: applied to biopsy tissue when culture is negative or when resistance is suspected.
• Work up for immunodeficiency in extensive, deep or recurrent disease: HIV testing, glycaemic assessment, review of drugs, and genetic testing for CARD9 deficiency when disease is invasive in a young person.

Treatment

Oral therapy is essential. Topical antifungal agents are added for the surrounding skin, and all topical corticosteroids are stopped.

Treatment is continued until lesions and the infiltrate have resolved and cultures are negative. Relapse occurs after early cessation. Treatment of tinea pedis and onychomycosis is part of cure, as these are the reservoir.

Additional management:

• Stop shaving and waxing the affected area until clear.
• Drainage or excision is rarely needed for abscess like lesions.
• In immunosuppressed hosts, reduce immunosuppression where possible, and monitor drug interactions between azoles and calcineurin inhibitors, with tacrolimus and ciclosporin levels checked. Terbinafine has fewer interactions with calcineurin inhibitors than itraconazole.
• Terbinafine resistant infection is treated with itraconazole, guided by susceptibility results.
• Lifelong secondary prophylaxis is considered in CARD9 deficiency and other inherited defects, with specialist advice.