Tinea Barbae Clinical Presentation

  • Author: Jacek C Szepietowski, MD, PhD; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Jan 23, 2012
 

History

  • 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.[3]
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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.

See the images below.

Inflammatory tinea barbae resulting from TrichophyInflammatory tinea barbae resulting from Trichophyton mentagrophytesvar granulosuminfection. Wax model of kerionlike tinea barbae. Courtesy of Wax model of kerionlike tinea barbae. Courtesy of the Museum of the Department of Dermatology, University of Medicine, Wroclaw, Poland.
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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.[4] 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.[5, 6] Microsporum canis and Trichophyton mentagrophytes var erinacei may cause tinea barbae but are rare.[7]

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.[8, 9, 10]

Other reported causative organisms include Trichophyton interdigitale[11] and Microsporum nanum.[12]

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Contributor Information and Disclosures
Author

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: Stiefel GSK Company Salary Employment; Orfagen Consulting fee Consulting; Maruho Consulting fee Consulting; Astellas Consulting fee Consulting; Abbott Consulting fee Consulting; Leo Pharma Consulting fee Consulting

Coauthor(s)

Robert A Schwartz, MD, MPH  Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, University of Medicine and Dentistry of New Jersey-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.

Specialty Editor Board

Franklin Flowers, MD  Chief, Division of Dermatology, Professor, Department of Medicine and Otolaryngology, Affiliate Associate Professor of Pediatrics and Pathology, 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.

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

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.

Paul Krusinski, MD  Director of Dermatology, Fletcher Allen Health Care; Professor, Department of Internal Medicine, University of Vermont College of Medicine

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.

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 Investigator; Genentech Grant/research funds investigator; Centocor Consulting fee Consulting; Abbott Grant/research funds investigator; Abbott Consulting fee Consulting; Novartis investigator; Pfizer Grant/research funds investigator; Celgene Consulting fee DMC Chair; NIAMS and NHLBI Grant/research funds investigator

Chief Editor

Dirk M Elston, MD  Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous Chief Editor, William D. James, MD, to the development and writing of this article.

References

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Inflammatory tinea barbae resulting from Trichophyton mentagrophytesvar granulosuminfection.
Wax model of kerionlike tinea barbae. Courtesy of the Museum of the Department of Dermatology, University of Medicine, Wroclaw, Poland.
 
 
 
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