Tinea barbae is a superficial dermatophyte infection that is limited to the bearded areas of the face and neck and occurs almost exclusively in older adolescent and adult males. The clinical presentation of tinea barbae includes inflammatory, deep, kerionlike plaques and noninflammatory superficial patches resembling tinea corporis or bacterial folliculitis. It may be viewed as an occupational disease among cattle farmers.[1]
Tinea barbae is caused by the keratinophilic fungi (dermatophytes) that are responsible for most superficial fungal skin infections. They infect the stratum corneum of the epidermis, hair, and nails. Several enzymes, including keratinases, are released by dermatophytes, which help them invade the epidermis. The mechanism that causes tinea barbae is similar to that of tinea capitis. In both diseases, hair and hair follicles are invaded by fungi, producing an inflammatory response. Tinea barbae is caused by both zoophilic and anthropophilic dermatophytes.
Infection caused by zoophilic dermatophytes usually is of greater severity than that produced by anthropophilic organisms. Thus, zoophilic dermatophytes are the primary cause of inflammatory kerionlike plaques, which most likely result from a more intense host reaction. Kerion formation has been described as resulting from Trichophyton rubrum infection.[2, 3, 4] T rubrum, an anthropophilic dermatophyte, can invade hair shafts and deeper tissues (although rarely), resulting in an inflammatory reaction. Usually, infection involving hair is more severe; therefore, tinea barbae caused by anthropophilic dermatophytes often has a more severe course than tinea corporis caused by the same pathogen.
Dermatomycoses may be due to pets and farm animals, sometimes from unusual dermatophytes. Trichophytonerinacei, a zoophilic dermatophyte occasionally harbored by hedgehogs, was linked with kerion-type tinea barbae in a 37-year-old man with the infection apparently transferred to his partner by direct contact from kissing.[5] Inflammatory tinea barbae was shown to be caused by Arthroderma benhamiae in both a patient and his guinea pig.[6]
The formation of kerion is postulated by 2 theories. The first theory suggests that it results from diffusion of metabolites and/or toxins from the fungus; however, kerion formation most likely results from an immunologic response to dermatophyte antigens.
Tinea barbae is caused by several dermatophytes, including zoophilic and anthropophilic organisms; however, zoophilic dermatophyte infection occurs more commonly. Frequently, animals (eg, cattle, horses, cats, dogs) constitute the source of infection.[7] Trichophyton species are most common, thus the term trichophytosis barbae also is used. Among zoophilic dermatophytes, Trichophyton mentagrophytes var granulosum and Trichophyton verrucosum are the most common causative agents.[8, 9, 10] Microsporum canis and Trichophyton mentagrophytes var erinacei may cause tinea barbae but are rare.[11]
T rubrum and Trichophyton violaceum are the most common anthropophilic dermatophytes responsible for tinea barbae; however, infections from Trichophyton megninii (endemic in Sardinia, Sicily, Portugal) and Trichophyton schoenleinii (endemic in Eurasia, Africa, Brazil) also may occur, especially in endemic regions. Infection of bearded skin by anthropophilic dermatophytes may be the result of autoinoculation from tinea pedis or onychomycosis.[12, 13, 14]
Other reported causative organisms include Trichophyton interdigitale[15] and Microsporum nanum.[16]
Currently, tinea barbae is infrequent around the world. As with other dermatophytoses, tinea barbae is more common in countries in which weather is characterized by high temperatures and humidity. It represented only 5.8% of dermatophytosis in one survey from the tropical region of southern Iran.[17]
Tinea barbae was observed more frequently in the past before single-use razors became available, and infection frequently was transmitted by barbers who used unsanitary razors. Therefore, it is not surprising that tinea barbae once was termed barber's itch. Now that habits and equipment have changed, this source of infection has been all but eliminated. Currently, tinea barbae is more common among rural inhabitants, and zoophilic dermatophytes constitute its primary pathogens. Dermatophytosis from zoophilic species of dermatophytes has increased in southwestern Iran, with the Trichophyton species of A benhamiae being a new cause in southwestern Iran.[18]
Sex
Men are affected almost exclusively by tinea barbae because the disease involves the bearded areas of the face and neck. Involvement of the same areas in healthy women and children is classified as tinea faciei.
Age
Hair appears on the face at puberty; therefore, tinea barbae may occur almost exclusively in older adolescent and adult males.
Prognosis usually is good for tinea barbae. Inflammatory lesions undergo spontaneous remission within a few months; however, if untreated, they leave scarring alopecia. Noninflammatory tinea barbae lesions are more likely to be chronic and may not tend to resolve spontaneously. In superficial chronic tinea barbae, alopecia may occur in the center of the lesions; however, this is not common.
Infection often begins on the chin or neck, but in severely affected patients, tinea barbae may cover the entire bearded area of the face and neck, occasionally resulting in indurated verrucous plaques or nodules.
Tinea barbae may be asymptomatic; however, mild pruritus is characteristic. Spontaneous resolution of tinea barbae may occur, especially in inflammatory tinea barbae.
Lupoid sycosis, a deep form of tinea barbae, is so named because it may resemble lupus vulgaris.[19]
Clinical manifestations of tinea barbae relate to the causative pathogen. Two clinical varieties of the disease are identified: inflammatory and noninflammatory.
Inflammatory deeper tinea barbae is caused primarily by zoophilic dermatophytes. This variety, termed a kerion, is the most common clinical presentation. Most patients show solitary plaques or nodules; however, multiple plaques are relatively common. Usually localized on the chin, cheeks, or neck, involvement of the upper lip is rare. The characteristic lesion is an inflammatory reddish nodule with pustules and draining sinuses on the surface. Hairs are loose or broken, and depilation is easy and painless. Pus-filled whitish masses involve the hair root and follicle. Over time, the surface of the indurated nodule is covered by exudate and crust. This variety of tinea barbae usually is associated with generalized symptoms, such as regional lymphadenopathy, malaise, and fever. Tinea barbae profunda may be due to a variety of fungi, including T mentagrophytes, A benhamiae, and M nanum.[6, 16, 20]
Noninflammatory superficial tinea barbae is caused by anthropophilic dermatophytes. This variety of barbae is less common and resembles common tinea corporis or bacterial folliculitis (sycosiform variety).[21] Typically, erythematous patches show an active border composed of papules, vesicles, and/or crusts. Hairs are broken next to the skin, or they plug the hair follicle. In the sycosiform variety, small follicular pustules are observed. Hairs are broken or loose. This variety represents a chronic variant of tinea barbae. Rarely, one may see tinea blepharociliaris associated with tinea barbae.[22]
See the images below.
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Inflammatory tinea barbae resulting from Trichophyton mentagrophytesvar granulosuminfection.
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Wax model of kerionlike tinea barbae. Courtesy of the Museum of the Department of Dermatology, University of Medicine, Wroclaw, Poland.
Mycologic features form the basis of tinea barbae diagnosis.[28] Procedures include direct microscopy, culture, and a Wood lamp examination showing fluorescence when Microsporum canis infection causes tinea barbae.
Specimen selection and collection is important. Usually, the material consists of infected hairs (depilated with forceps) and pustular masses. In the superficial variety, which resembles tinea corporis, collect scrapings from the border of the lesion where the inflammatory reaction is more severe. Taking material from the lesion's border increases the possibility of detecting fungi on direct microscopy and culture. Send the specimen for culture, or examine it for fungus.
Direct microscopic examination is performed rapidly and easily; however, it requires experience. Place the material on a slide and add a solution of 10-20% potassium hydroxide, with or without dimethyl sulfoxide. This solution provides visualization of fungal elements. Gently warm the slide, especially if no dimethyl sulfoxide is added. Some recommend using special stains, such as chlorazol black E stain or Parker blue-black ink. Direct microscopy usually shows hyphae and/or arthroconidia. Wait for some minutes before evaluating the preparation under microscopy, or reexamine the slide after one-half hour, since fungal elements may be difficult to see just after addition of potassium hydroxide solution.
Culture identifies the causative fungus and usually is performed on Sabouraud agar with the addition of cycloheximide and chloramphenicol. These two substances inhibit bacterial and other fungal growth to obtain pure dermatophyte colonies. Cultures take approximately 3 weeks to become positive, and final fungal identification is based primarily on morphology and microscopy of the colonies. Occasionally, additional tests are required. Special media for rapid dermatophyte identification that include a color indicator currently are available. In the presence of dermatophytes, the color changes from yellow to bright red.
Biopsy specimens occasionally may be required to diagnose tinea barbae. Biopsy shows folliculitis and perifolliculitis with a mixed cellular infiltrate and spongiotic alterations within the follicular epithelium. Lymphocytes or neutrophils also may be evident within follicular epithelium. Neutrophils also may be seen within follicular keratin as microabscesses.
Since fungal elements often are difficult to visualize with hematoxylin and eosin stain, periodic acid-Schiff stain is recommended. Arthroconidia and/or hyphae may be evident within the hair shaft and in the hair follicle. An inflammatory infiltrate is present in the dermis, which in chronic lesions may contain giant cells.
Since hairs are infected in tinea barbae, the therapeutic procedure is similar to that of tinea capitis. Shaving or hair depilation is recommended with warm compresses to remove crusts and debris. Topical formulations with antifungal compounds (eg, shampoo, lotion, cream) can be applied, but tinea barbae requires oral antifungal therapy. Details of therapeutic modalities for tinea barbae are found in Medication.
Griseofulvin remains in wide use. Newer antifungals, especially terbinafine,[29] also can be used. At the author's institution, experience with terbinafine in tinea barbae has been excellent, with all cures achieved within 4 weeks of initiating therapy. Itraconazole can be recommended as one-pulse therapy at a dosage of 400 mg/d divided into 2 doses for 1 week. Some prefer to use a second pulse after 3 weeks. Itraconazole also may be used continuously for 4 weeks at a dose of 200 mg/d. Fluconazole treatment is not well documented, but data from tinea capitis studies indicate that a dose of 150 mg once per week for up to 6 weeks also may be effective. All of these new antifungal drugs generally are well tolerated.
Eliminating the source of tinea barbae infection is of great importance. If farm workers become infected, examine all animals for the presence of fungal skin lesions. Treatment of other fungal skin infections, such as tinea pedis or onychomycosis, may prevent the infection's spread by autoinoculation.
Clinical Context:
Griseofulvin has fungistatic activity. Fungal cell division is impaired by interfering with the microtubule. Griseofulvin binds to keratin precursor cells. Keratin is gradually replaced by noninfected tissue, which is highly resistant to fungal invasions.
Clinical Context:
Terbinafine is a member of the allylamine family and a fungicidal agent that inhibits ergosterol synthesis via squalene epoxidase, which results in a decreased ergosterol level and an increased concentration of squalene; this leads to cell death. Use medication until symptoms significantly improve.
Clinical Context:
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.
Clinical Context:
Fluconazole has fungistatic activity. It is a synthetic oral antifungal (broad-spectrum bistriazole) that selectively inhibits fungal cytochrome P-450 and sterol C-14 alpha-demethylation, which prevents conversion of lanosterol to ergosterol, thereby disrupting cellular membranes.
The mechanism of action usually involves inhibiting pathways (enzymes, substrates, transport) necessary for sterol/cell membrane synthesis or altering the permeability of the cell membrane (polyenes) of the fungal cell.
Robert A Schwartz, MD, MPH, Professor and Head of Dermatology, Professor of Pathology, Professor of Pediatrics, Professor of Medicine, Rutgers New Jersey Medical School
Disclosure: Nothing to disclose.
Coauthor(s)
Jacek C Szepietowski, MD, PhD, Professor, Vice-Head, Department of Dermatology, Venereology and Allergology, Wroclaw Medical University; Director of the Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Poland
Disclosure: Received consulting fee from Orfagen for consulting; Received consulting fee from Maruho for consulting; Received consulting fee from Astellas for consulting; Received consulting fee from Abbott for consulting; Received consulting fee from Leo Pharma for consulting; Received consulting fee from Biogenoma for consulting; Received honoraria from Janssen for speaking and teaching; Received honoraria from Medac for speaking and teaching; Received consulting fee from Dignity Sciences for consulting; .
Specialty Editors
Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Disclosure: Nothing to disclose.
Paul Krusinski, MD, Director of Dermatology, Fletcher Allen Health Care; Professor, Department of Internal Medicine, University of Vermont College of Medicine
Disclosure: Nothing to disclose.
Chief Editor
William D James, MD, Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine
Disclosure: Received income in an amount equal to or greater than $250 from: Elsevier; WebMD.
Additional Contributors
Franklin Flowers, MD, Department of Dermatology, Professor Emeritus Affiliate Associate Professor of Pathology, University of Florida College of Medicine
Szepietowski JC, Bielicka E, Maj J. Inflammatory tinea barbae due to Trichophyton rubrum infection - autoinnoculation from fingernail onychomycosis?. Case Rep Clin Pract Rev. 2002. 3:254-6.
Szepietowski JC, Matusiak L. Trichophyon rubrum autoinoculation from infected nails is not such a rare phenomenon. Mycoses. 2008. 51:345-346.
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