Tinea Barbae

Etiology

Transmission of dermatophytes to humans occurs via direct contact with infected humans (anthropophilic), soil (geophilic), or infected animals (zoophilic).[7] Research has revealed that tinea barbae is caused exclusively by zoophilic and anthropophilic dermatophytes.[1] Trichophyton verrucosum, Trichophyton mentagrophytes, and Trichophyton rubrum are the most commonly reported causative organisms.[1][7][8][9][10][11] Other documented causative organisms include Trichophyton violaceum, Trichophyton megninii, Trichophyton schoenleinii, Trichophyton tonsurans, Trichophyton interdigitale, Trichophyton ernacei, Microsporum canis, Microsporum nanum, Mycroscporum gypseum, and Epidermophyton floccosum.[1] However, infections from Trichophyton megninii (endemic in Sardinia, Sicily, and Portugal) and Trichophyton schoenleinii (endemic in Eurasia, Africa, and Brazil) may also occur, particularly in endemic regions. T rubrum and T violaceum are the most common anthropophilic dermatophytes responsible for tinea barbae.

Pets, domestic animals, and uncommon dermatophytes may cause dermatomycoses. Until 2000, most of the tinea barbae cases documented in the literature were caused by zoophilic dermatophytes from infected farm animals and domestic animals, especially dairy cows (T verrucosum), sheep, pigs (T ernacei), horses, dogs, and cats (Microsporum canis).[1][12] More recently, infections with anthropophilic T rubrum have been frequently reported, as noted in multiple individual case reports worldwide and case series published from Portugal and Mexico.[1][8][9][10][11] T erinacei, a zoophilic dermatophyte occasionally found in hedgehogs, was associated with kerion-type tinea barbae in a 37-year-old male. The infection was reportedly transmitted to his partner through direct mouth-to-mouth contact.[12] Trichophyton benhamiae, previously known as Arthroderma, was identified as the cause of inflammatory tinea barbae in both a patient and his guinea pig.[13] Though it is still considered a rare cause of tinea barbae, T benhamiae is an emergent zoophilic dermatophyte that has been reported worldwide, particularly in children.[14]

Human-to-human transmission of tinea barbae is rare but possible. Recent individual case reports document autoinoculations with T rubrum in patients with tinea pedis.[8][9][10] Trichophyton tonsurans may cause tinea barbae after shaving with insufficiently disinfected hairdressing instruments. Autoinoculation from onychomycosis may also result in the infection of bearded skin by anthropophilic dermatophytes.[15]

The severity of infection caused by zoophilic dermatophytes is typically greater than that caused by anthropophilic organisms. Thus, inflammatory kerion-like lesions are primarily caused by zoophilic dermatophytes, likely resulting from a more severe host reaction. Kerion formation has been characterized as a consequence of an infection with T rubrum and a T mentagrophytes complex. T rubrum, an anthropophilic dermatophyte, can enter hair shafts and rarely deeper tissues, causing an inflammatory reaction. Typically, infections that affect hair are more severe. Consequently, tinea barbae, caused by anthropophilic dermatophytes, frequently has a more severe course than tinea corporis caused by the same pathogen.[16]

Epidemiology

Though superficial fungal infections are common worldwide, tinea barbae is relatively uncommon. Tinea barbae was first reported in 1842 by Gruby, and since then, only a little over 150 cases have been reported in the literature until 1990.[1] Most of the data since 1990 about tinea barbae are either isolated case reports or small case series.[1] 

Tinea barbae is more prevalent in countries with high temperatures and humidity, similar to other dermatophytoses. Tinea barbae was more frequently observed before the availability of single-use razors, and barbers who used unhygienic razors often transmitted the infection. Consequently, it is unsurprising that tinea barbae was previously referred to as barber's rash. This source of infection has been nearly eradicated due to the modifications to equipment and behaviors. Currently, tinea barbae is more prevalent among rural residents, and its primary pathogens are zoophilic dermatophytes.[17]

Due to the rarity of the disease, predicting a true incidence or lifetime risk is difficult. Dermatophytes are distributed worldwide, and so are the reported cases of tinea barbae. Since tinea barbae is an infection of the hair and hair follicles of the beard and mustache area, it is exclusively seen in adolescent boys and men. In an extreme rarity, a case of tinea barbae was reported in a hirsute woman in a longitudinal study from Portugal.[11]

Pathophysiology

Dermatophytes are keratinophilic fungi that cause superficial and deep infections of the keratinized tissues. The dryness of the skin’s outer layer, shedding of the outer layers of the dead skin, and the innate peptides and medium-chain fatty acids secreted onto the skin generally prevent the colonization of the microorganisms.[3][18] However, certain factors like age, immune status, steroid use, diabetes, trauma, and occupational exposures increase the likelihood of dermatophyte infections.[3][18]

Dermatophytes and the host's inflammatory response are responsible for the pathology.[3] Both fungal-specific and host-specific factors play a role in the inflammatory process. The fungal-specific factors responsible for pathogenesis are adaptation to the specific host, release of enzymes, production of inflammatory factors and toxins, and release of immunomodulating agents. The host-specific factors that play a role in the inflammation process are the site of entry, nonspecific defense mechanisms, and the immune response. 

Two hypotheses propose the formation of kerion. The initial theory proposes that kerion formation results from the diffusion of metabolites and toxins from the fungus. However, it is more probable that kerion formation results from an immunologic response to dermatophyte antigens. The infection begins with inoculating the arthroconidium (spores) to the keratinized tissue. Once inoculated, the carbohydrate microfibrils on the fungal spores anchor to the keratinocytes. Once anchored, the spores germinate and produce hyphae, which spread centrifugally into the deeper layers of the stratum corneum.[3][19] Invading fungal hyphae produce keratinases, proteases, elastases, and other pathogenic factors into the stratum corneum. These enzymes help in the digestion and utilization of the keratin and other proteins needed for the survival and growth of the dermatophytes.[3] Dermatophytes develop a specialized structure called the penetrating organ to invade the hair shafts.[3] Keratinases activate the keratinocytes to release inflammatory mediators like cytokines and interleukins. The interleukins and cytokines released by the keratinocytes will recruit both humoral and cell-mediated immune responses depending on the specific pathogen.[19]

Histopathology

Occasionally, it may be necessary to obtain biopsy specimens to diagnose tinea barbae. A mixed cellular infiltrate and spongiotic alterations within the follicular epithelium are evident in the biopsy, which also reveals folliculitis and perifolliculitis. Additionally, lymphocytes or neutrophils may be observed in the follicular epithelium. Neutrophils may also be observed as microabscesses within follicular keratin.Hematoxylin and eosin stain are frequently inadequate for visualizing fungal elements; periodic acid-Schiff stain is advised. Arthroconidia and hyphae may be visible in the hair shaft and hair follicle. In chronic lesions, an inflammatory infiltrate is present in the dermis, which may contain giant cells.

History and Physical

As tinea barbae is a relatively rare dermatophyte infection, awareness of the disease and a thorough medical history will help make a prompt diagnosis. Zoophilic fungi predominantly cause tinea barbae; occupational history and contact with pets or domesticated animals will help narrow the differential diagnosis. Factors like diabetes, local trauma, steroid use, and immunosuppressive therapy can suppress local defense mechanisms and predispose them to infections with dermatophytes.[1] Considering that there have been multiple cases of anthropophilic dermatophytoses via autoinoculation and transmission from person to person, it is important to know the history of other dermatophyte infections like tinea capitis or tinea pedis in the patient or their close contacts.[20]

Clinically, tinea barbae presents as 2 different morphologies, inflammatory and noninflammatory.[1][6][19] The classic inflammatory form of tinea barbae, often seen with zoophilic dermatophytosis, develops a characteristic lesion called a kerion. Kerion is an erythematous, boggy, tender, often sterile, weeping nodule or plaque with pustules and draining sinuses.[6][7] Most patients exhibit solitary plaques or nodules; multiple plaques are relatively common. Involvement of the upper lip is uncommon; tinea barbae is typically restricted to the jawline, cheeks, or neck. Hairs are either loose or damaged, and depilation is a painless and simple process. The hair root and follicle are involved in pus-filled whitish masses. The indurated nodule's surface is gradually obscured by exudate and crust.

Tinea barbae profunda may be caused by various fungi, such as T mentagrophytes, T benhamiae, and Microsporum nanum.[6][7] Generalized symptoms, including regional lymphadenopathy, malaise, and fever, are typically associated with this tinea barbae variety.[6] Kerion is a coalesced sterile pustule, but occasionally, it can get superinfected with cutaneous bacteria and develop regional lymphadenopathy.[7]  

Noninflammatory superficial tinea barbae is induced by anthropophilic dermatophytes. This variant of barbae is rarer and resembles typical tinea corporis or bacterial folliculitis (sycosiform type). Erythematous patches generally exhibit an active border of papules, vesicles, or crusts. Hairs are fractured adjacent to the skin or clog the hair follicle. Small follicular pustules are found in the sycosiform variant. Hairs are fractured or detached; this type signifies a chronic form of tinea barbae.[6][7]

Evaluation

Tinea barbae is often diagnosed clinically. Knowledge about the disease, its clinical presentation, and a thorough history and physical examination can help in early diagnosis. Since the mainstay of treatment for tinea barbae is systemic antifungal therapy for an extended period with potential adverse events, it is important to verify the diagnosis. Simple, inexpensive in-office testing can establish the diagnosis, such as direct microscopic examination of skin scrapings from the lesion or direct visualization of the affected area under a Wood lamp. However, visualization of the affected area under the Wood lamp is limited, as most dermatophytes that cause tinea barbae do not fluoresce, except for Microsporum.[1] 

Direct Microscopic Examination

Obtain scales and skin scrapings from the active border of the lesion by using a scalpel or moist cotton tip along with epilated hairs. Transfer the collected sample onto a slide and add 10% to 20% potassium hydroxide solution drops. To speed up the emulsification of the skin cells, gently warm the slide or add dimethyl sulfoxide.[7][20] Fungal stains such as chlorazol black E or Parker blue-black ink may be added to the sample to highlight the fungal elements.[20] Examining the wet-mount preparation under 20- and 40-times magnification will reveal branching, rod-shaped fungal filaments with uniform width (hyphae) and minute spores (arthroconidia), which are diagnostic.[7][18] Depending on the causative organism, fungal elements can be observed covering the hair (ectothrix) or invading the hair shaft (endothrix).[7]

Fungal Culture

Innoculate the collected skin scrapings and hair samples into the specialized dermatophyte test medium. Mycocel™ and mycobiotic agar are commercially available test media for dermatophytes. These specialized media have cycloheximide and chloramphenicol to inhibit contaminating fungi and bacteria growth.[7] These test media also have phenol red as an indicator, which turns from yellow to pinkish-red in the presence of alkaline metabolites of dermatophytes.[7][18][20] The fungus takes 7 to 14 days to grow on this medium; the inoculated medium should show no growth for 21 days before declaring the culture negative.[18] Based on the colony and microscopic morphology, individual species responsible for dermatophytoses can be differentiated. Fungal cultures are time-consuming and expensive but have better sensitivity and specificity than direct microscopy. A fungal culture is not mandatory before initiating antifungal therapy but helps determine the treatment's appropriateness.

Skin Biopsy and Histopathological Examination

Direct microscopic examination or fungal cultures can diagnose most tinea barbae infections. Skin biopsy and histopathological examination of the tissue are reserved for cases refractory to treatment or where other methods can not establish a definitive diagnosis.[20] Periodic acid-Schiff (PAS) stain is recommended as fungal elements are often not differentiated with hematoxylin and eosin staining.[6] Microscopy under PAS stain shows fungal hyphae, arthroconidia, and inflammatory changes in the epidermis and dermis. Inflammatory patterns in the biopsy sections are consistent with folliculitis, perifolliculitis, and microabscesses.

Conventional diagnostic methods mentioned above are adequate for diagnosing tinea barbae but may not be specific to identify the exact causative pathogen by species. Newer diagnostic modalities like polymerase chain reaction-restriction fragment length polymorphism on the ribosomal deoxyribonucleic acid internal transcribed spacer region will help determine the specific pathogen. Currently, specialized centers primarily studying epidemiology, transmission patterns, and drug development can only afford these expensive tests.[2]

Treatment / Management

The mainstay of treatment for tinea barbae is oral antifungal therapy. Topical agents can be used, but only as an adjunct therapy.[20] Oral antifungal agents that have proven effective in the management of tinea barbae are terbinafine, azoles, and griseofulvin.[20] Griseofulvin used to be the preferred drug, but it is rarely used now due to its adverse events, drug resistance, need for prolonged therapy, and increased relapse rates due to the rapid clearance of the drug from the skin.[7][18] (A1)

In the past, tinea barbae was treated for 12 weeks with griseofulvin. Recent case reports have demonstrated complete resolution of the tinea barbae with 4 to 6 weeks of therapy with terbinafine and azoles.[5][8][9][10][11] Even though 4 weeks of treatment are sufficient, some authors have suggested continuing treatment for 2 to 3 weeks after the resolution of the lesions.(B3)

Recommended dosages for the available antifungal agents for tinea barbae are:

• Terbinafine 125 mg to 250 mg once daily
• Ketoconazole 200 mg to 400 mg daily
• Fluconazole 200 mg once daily
• Itraconozole 100 mg oncedaily

Common adverse events of terbinafine and azoles include nausea, abdominal pain, diarrhea, rash, elevated transaminases, and visual disturbances.[7] Periodic monitoring of hepatic, renal, and hematopoietic function is recommended for patients taking systemic antifungal therapy. Significant drug interactions can happen when hepatically metabolized drugs are taken along with azoles.[7] (B3)

The role of steroids and other topical agents like selenium sulfide as a treatment for tinea barbae is not well defined, and it is the prescriber’s discretion on a case-by-case basis. Suspecting a secondary bacterial infection warrants the use of oral or systemic antibiotics. Surgery is rarely indicated, and incision and drainage of kerion are not recommended.[20](A1)

Dermatophyte infections resistant to antifungal agents are a significant global health issue.[21] Photodynamic therapy that is 5-aminolevulinic acid-based is a recent alternative that circumvents the adverse events and drug resistance of conventional antifungal agents.[22]

Differential Diagnosis

Tinea barbae is a rare disease frequently misdiagnosed as a common condition affecting the beard and mustache area.[3] Knowing the common characteristics that can differentiate tinea barbae from other conditions clinically to aid with prompt diagnosis is important. Bacterial folliculitis caused by Staphylococcus species or other bacteria can be differentiated from tinea barbae by systemic symptoms like fever and malaise. Regional lymphadenopathy is more common with bacterial folliculitis, and hair removal is painless in tinea barbae compared to bacterial folliculitis. Pseudofolliculitis barbae is a form of irritant folliculitis caused secondary to shaving, and its presentation is bilateral and diffuse compared to tinea barbae. Candidal folliculitis can be differentiated from tinea barbae by the involvement of adjacent mucosal surfaces.

Other differential diagnoses include:

• Lupus vulgaris may mimic lupoid sycosis, a deep variant of tinea barbae
• Bockhart impetigo
• Carbuncles
• Pustular syphilis
• Nodulocystic acne
• Iododerma
• Bromoderma
• Papulopustular rosacea
• Perioral dermatitis
• Herpes simplex
• Sporotrichosis
• Contact dermatitis
• Neoplasm

Prognosis

Tinea barbae is a rare dermatophytic infection, with only a few hundred cases reported in the literature. Most reported cases are either single-case reports or small case series. Though the data available is limited, it has been very reassuring, as almost all cases responded well to oral antifungal therapy and resolved completely.

Inflammatory lesions typically resolve spontaneously within a few months; however, if left untreated, they can result in scarring alopecia. Noninflammatory tinea barbae lesions are more likely to be chronic and may not resolve spontaneously. Alopecia may manifest in the center of the lesions of superficial chronic tinea barbae; however, this is uncommon.

Complications

The literature has not reported any significant complications other than morbidity and healthcare costs related to the therapy.