eMedicine Specialties > Dermatology > Fungal Infections

Tinea Barbae

Author: Jacek C Szepietowski, MD, PhD, Professor and Vice-Head, Department of Dermatology, Venereology and Allergology, Wroclaw Medical University, Poland
Coauthor(s): Robert A Schwartz, MD, MPH, Professor and Head of Dermatology, Professor of Medicine, Professor of Pediatrics, Professor of Pathology, Professor of Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
Contributor Information and Disclosures

Updated: Feb 27, 2007

Introduction

Background

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.

Pathophysiology

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. Recently, kerion formation has been described as resulting from Trichophyton rubrum infection. 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.

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.

Frequency

United States

Tinea barbae is uncommon in the United States.

International

Currently, tinea barbae is infrequent around the world. As with other dermatophytoses, it is more common in countries in which weather is characterized by high temperatures and humidity. 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.

Mortality/Morbidity

Permanent alopecia and scarring frequently follow spontaneous resolution of inflammatory plaques and nodules. In superficial chronic tinea barbae, alopecia may occur in the center of the lesions; however, this is not common.

Sex

Men are affected almost exclusively 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.

Clinical

History

  • Infection often begins on the chin or neck, but in severely affected patients, it 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 may occur, especially in inflammatory tinea barbae.
  • Lupoid sycosis, a deep form of tinea barbae, is so named because it may resemble lupus vulgaris.

Physical

Clinical manifestations of tinea barbae relate to the causative pathogen. Two clinical varieties of the disease are identified as follows:

  • 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.
  • 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). 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.

Causes

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. 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. Microsporum canis and Trichophyton mentagrophytes var erinacei may cause tinea barbae but are rare.

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.

More on Tinea Barbae

Overview: Tinea Barbae
Differential Diagnoses & Workup: Tinea Barbae
Treatment & Medication: Tinea Barbae
Follow-up: Tinea Barbae
Multimedia: Tinea Barbae
References

References

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Further Reading

Keywords

ringworm of the beard, barber's itch, trichophytosis barbae, tinea sycosis, sycosis

Contributor Information and Disclosures

Author

Jacek C Szepietowski, MD, PhD, Professor and Vice-Head, Department of Dermatology, Venereology and Allergology, Wroclaw Medical University, Poland
Disclosure: Stiefel Salary Employment

Coauthor(s)

Robert A Schwartz, MD, MPH, Professor and Head of Dermatology, Professor of Medicine, Professor of Pediatrics, Professor of Pathology, Professor of Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi
Disclosure: Nothing to disclose.

Medical Editor

Franklin Flowers, MD, Chief, Division of Dermatology, Professor, Department of Medicine and Otolaryngology, University of Florida College of Medicine
Franklin Flowers, MD is a member of the following medical societies: American College of Mohs Micrographic Surgery and Cutaneous Oncology
Disclosure: Nothing to disclose.

Pharmacy Editor

Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Paul Krusinski, MD, Director of Dermatology, Professor, Department of Internal Medicine, Fletcher Allen Health Care, University of Vermont
Paul Krusinski, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

CME Editor

Joel M Gelfand, MD, MSCE, Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania
Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology
Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds None; Genentech Consulting fee Consulting; Centocor Consulting fee Consulting; Centocor Grant/research funds None; Covance Consulting fee Consulting; Shire  Consulting

Chief Editor

William D James, MD, Paul R Gross Professor of Dermatology, University of Pennsylvania School of Medicine; Vice-Chair, Program Director, Department of Dermatology, University of Pennsylvania Health System
William D James, MD is a member of the following medical societies: American Academy of Dermatology and Society for Investigative Dermatology
Disclosure: elsevier Royalty Other; american college of physicians Honoraria Other

 
 
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