eMedicine Specialties > Dermatology > Fungal Infections

Tinea Barbae

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
Coauthor(s): Robert A Schwartz, MD, MPH, Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
Contributor Information and Disclosures

Updated: Sep 25, 2009

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. Kerion formation has been described as resulting from Trichophyton rubrum infection.1,2 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, tinea barbae 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 the inflammatory plaques and nodules of tinea barbae. 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 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.

Clinical

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

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.
Inflammatory tinea barbae resulting from <EM>Tric...

Inflammatory tinea barbae resulting from Trichophyton mentagrophytes var granulosum infection.

Inflammatory tinea barbae resulting from <EM>Tric...

Inflammatory tinea barbae resulting from Trichophyton mentagrophytes var granulosum infection.


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.

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.


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 interdigitale11 and Microsporum nanum.12

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

  1. Beswick SJ, Das S, Lawrence CM, Tan BB. Kerion formation due to Trichophyton rubrum. Br J Dermatol. Nov 1999;141(5):953-4. [Medline].

  2. Gupta G, Burden AD, Roberts DT. Acute suppurative ringworm (kerion) caused by Trichophyton rubrum. Br J Dermatol. Feb 1999;140(2):369-70. [Medline].

  3. Bonifaz A, Ramirez-Tamayo T, Saul A. Tinea barbae (tinea sycosis): experience with nine cases. J Dermatol. Dec 2003;30(12):898-903. [Medline].

  4. Davis DF, Petri WH, Hood AF. Dairy farmer with a rapidly enlarging lip lesion: tinea barbae. Arch Dermatol. Aug 2006;142(8):1059-64. [Medline].

  5. Kiska DL, Cynamon MH. Photo quiz. Tinea barbae caused by Trichophyton verrucosum. Clin Infect Dis. Oct 1997;25(4):805, 871. [Medline].

  6. Maeda M, Nakashima T, Satho M, Yamada T, Kitajima Y. Tinea barbae due to Trichophyton verrucosum. Eur J Dermatol. May-Jun 2002;12(3):272-4. [Medline].

  7. Kick G, Korting HC. Tinea barbae due to Trichophyton mentagrophytes related to persistent child infection. Mycoses. Nov 1998;41(9-10):439-41. [Medline].

  8. Kawada A, Aragane Y, Maeda A, Yudate T, Tezuka T, Hiruma M. Tinea barbae due to Trichophyton rubrum with possible involvement of autoinoculation. Br J Dermatol. May 2000;142(5):1064-5. [Medline].

  9. 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. [Full Text].

  10. Szepietowski JC, Matusiak L. Trichophyon rubrum autoinoculation from infected nails is not such a rare phenomenon. Mycoses. 2008;51:345-346.

  11. Trotha R, Graser Y, Platt J, et al. Tinea barbae caused by a zoophilic strain of Trichophyton interdigitale. Mycoses. Feb 2003;46(1-2):60-3. [Medline].

  12. Ratka P, Slusarczyk E, Sloboda T, Kusmierski W. [Case of tinea barbae profunda caused by Microsporum nanum]. Przegl Dermatol. Sep-Dec 1983;70(5-6):549-52. [Medline].

  13. Kapdagli H, Ozturk G, Dereli T, et al. Candida folliculitis mimicking tinea barbae. Int J Dermatol. Apr 1997;36(4):295-7. [Medline].

  14. Kurita M, Kishimoto S, Kibe Y, Takenaka H, Yasuno H. Candida folliculitis mimicking tinea barbae. Acta Derm Venereol. Mar-Apr 2000;80(2):153-4. [Medline].

  15. Baran W, Szepietowski JC, Schwartz RA. Tinea barbae. Acta Dermatoven APA. 2004;13:91-4. [Full Text].

  16. Tanuma H, Doi M, Nishiyama S, Katsuoka K. A case of tinea barbae successfully treated with terbinafine. Mycoses. Jan-Feb 1998;41(1-2):77-81. [Medline].

  17. Kwasniewska J. Current antifungal agents in dermatology. Postepy Dermatol (Poznan). 1997;14:129-35.

  18. Bihari A, Simon G. Tinea barbae profunda. Borgyogyaszati Venerol Szemle (Budapest). 1998;74:283-6.

  19. Ceburkovas O, Schwartz RA, Janniger CK. Tinea capitis: current concepts. J Dermatol. Mar 2000;27(3):144-8. [Medline].

  20. De Lacerda MH, Caldeira JB, Delfino JP, Nunes FP, Goncalves H, Lobo C. [Sycosis of the beard (tinea barbae). Analysis of 42 cases]. Med Cutan Ibero Lat Am. 1981;9(3):161-78. [Medline].

  21. Foti C, Diaferio A, Daddabbo M, Angelini G. Tinea barbae associated with erythema nodosum in an immunocompetent man. J Eur Acad Dermatol Venereol. May 2001;15(3):250-1. [Medline].

  22. Glaser DA, Riordan AT. Images in clinical medicine. Tinea barbae: man and beast. N Engl J Med. Mar 12 1998;338(11):735. [Medline].

  23. Krajewska-Kulak E, Niczyporuk W, Lukaszuk C, Bartoszewicz M, Roszkowska I, Edyta M. Difficulties in diagnosing and treating tinea in adults at the Department of Dermatology in Bialystok (Poland). Dermatol Nurs. Dec 2003;15(6):527-30, 534. [Medline].

  24. Macura AB. Resistance to antimycotic drugs. Postepy Dermatol (Poznan). 1997;14:137-40.

  25. Michalowski R, Kuczynska L. [Initial experiences with a natamycin-, neomycin-, and hydrocortisone-containing lotion in tinea barbae]. Mykosen. Mar 1984;27(3):153-6. [Medline].

  26. Sander CS, Sander O, Khatib A, Berger T. Tinea barbae spreading to locus minoris resistentiae. Eur J Dermatol. Mar-Apr 2009;19(2):173-4. [Medline].

  27. Soyer HP, Cerroni L. The significance of histopathology in the diagnosis of dermatomycoses. Acta Derm Venerol (Ljubljana). 1992;1:84-7.

Further Reading

Keywords

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

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 Salary Employment; Orfagen Consulting fee Consulting; Maruho Consulting fee Consulting; Astellas 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, 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

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.