You are in: eMedicine Specialties > Dermatology > FUNGAL INFECTIONS Tinea BarbaeArticle Last Updated: Feb 27, 2007AUTHOR AND EDITOR INFORMATIONSection 1 of 11
  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 Editors: Franklin Flowers, MD, Chief, Division of Dermatology, Professor, Department of Medicine and Otolaryngology, University of Florida College of Medicine; Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University School of Medicine; Consulting Staff, Mountain View Dermatology, PA; Paul Krusinski, MD, Director of Dermatology, Professor, Department of Internal Medicine, Fletcher Allen Health Care, University of Vermont; 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; 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 Author and Editor Disclosure Synonyms and related keywords: ringworm of the beard, barber's itch, trichophytosis barbae, tinea sycosis, sycosis INTRODUCTIONSection 2 of 11
  BackgroundTinea 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. PathophysiologyTinea 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. FrequencyUnited StatesTinea barbae is uncommon in the United States. InternationalCurrently, 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/MorbidityPermanent 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. SexMen 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. AgeHair appears on the face at puberty; therefore, tinea barbae may occur almost exclusively in older adolescent and adult males. CLINICALSection 3 of 11
History
PhysicalClinical manifestations of tinea barbae relate to the causative pathogen. Two clinical varieties of the disease are identified as follows:
CausesTinea 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. DIFFERENTIALSSection 4 of 11
Acne Vulgaris Actinomycosis Candidiasis, Cutaneous Contact Dermatitis, Allergic Contact Dermatitis, Irritant Folliculitis Rosacea Syphilis
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| Drug Name | Griseofulvin (Fulvicin P/G, Grifulvin V) |
|---|---|
| Description | Fungistatic activity. Fungal cell division is impaired by interfering with microtubule. Binds to keratin precursor cells. Keratin is gradually replaced by noninfected tissue, which is highly resistant to fungal invasions. |
| Adult Dose | 500 mg microsize (330-375 mg ultramicrosize) PO qd or bid, continue for 2 wk after clinical lesions resolve |
| Pediatric Dose | Suggested dose: 20 mg microsize/kg/d (5 mg/lb/d) PO or 7.3 mg ultramicrosize/kg/d (3.3 mg/lb/d) PO |
| Contraindications | Documented hypersensitivity; hepatic injury |
| Interactions | Reduced effects of cyclosporine, salicylates, and warfarin (decreased hypoprothrombinemic activity); avoid alcohol use, since disulfiramlike reaction may occur; intense UV light exposure may result in phototoxic reaction; contraceptives may lose their effectiveness |
| Pregnancy | C - Safety for use during pregnancy has not been established. |
| Precautions | Better absorption when taken with fatty food; adverse effects may include abdominal pain, nausea, diarrhea, headache, and rarely, Stevens-Johnson syndrome and photodermatitis; 20% of patients experience adverse effects with griseofulvin; in prolonged therapy, observe patients closely; monitor renal, hepatic, and hematopoietic function regularly |
| Drug Name | Terbinafine (Lamisil) |
|---|---|
| Description | Member of allylamine family and a fungicidal agent that inhibits ergosterol synthesis via squalene epoxidase, which results in decreased ergosterol level and increased concentration of squalene; leads to cell death. Use medication until symptoms significantly improve. |
| Adult Dose | 250 mg/d PO for 4 wk |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity |
| Interactions | Cimetidine, rifampin, and cyclosporine rarely may interact; toxicity may increase with coadministration of rifampin and cimetidine; coadministration with cyclosporine may decrease cyclosporine level |
| Pregnancy | B - Usually safe but benefits must outweigh the risks. |
| Precautions | Generally well tolerated; adverse effects are primarily GI, including hepatobiliary dysfunction; transient loss of sense of taste is rare but specific adverse effect; blood dyscrasias, Stevens-Johnson syndrome, and ocular disturbances are described; minimally inhibits cytochrome P450 enzyme pathway |
| Drug Name | Itraconazole (Sporanox) |
|---|---|
| Description | Fungistatic activity. 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. |
| Adult Dose | 400 mg/d PO divided bid for 1 wk or 200 mg/d PO divided bid for 4 wk; not to exceed 400 mg/d; increase in 100-mg increments if no improvement |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; coadministration with lovastatin, simvastatin, cisapride, triazolam, or midazolam; coadministration with cisapride may cause arrhythmia; coadministration with triazolam and midazolam may increase plasma levels; rhabdomyolysis may occur with coadministration of HMG-CoA reductase inhibitors |
| Interactions | Frequent: increased level of cyclosporine, tacrolimus, and digoxin may occur after coadministration; phenytoin and rifampin may decrease effect; amlodipine and nifedipine taken concurrently may cause edema; hypoglycemia was observed after coadministration with sulfonylureas; avoid alcohol use, since disulfiramlike reactions may occur; antacids may reduce absorption; coadministration with terfenadine (recalled from US market), astemizole (recalled from US market), lovastatin, simvastatin, cisapride, triazolam, and midazolam; serious cardiovascular events, including death, were reported in patients treated with itraconazole and H1-receptor inhibitors (terfenadine, astemizole); coadministration with cisapride may cause arrhythmia; coadministration with triazolam and midazolam may increase their plasma levels; rhabdomyolysis may occur with coadministration of HMG-CoA reductase inhibitors (lovastatin, simvastatin) |
| Pregnancy | C - Safety for use during pregnancy has not been established. |
| Precautions | Generally well tolerated, but approximately 12% of patients may have adverse effects including GI abnormalities; hepatobiliary dysfunction has been observed; recommended to be taken with fatty food, which increases absorption from alimentary tract |
| Drug Name | Fluconazole (Diflucan) |
|---|---|
| Description | Fungistatic activity. 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. |
| Adult Dose | 150 mg PO qwk for up to 6 wk |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity |
| Interactions | Levels may increase with hydrochlorothiazide; fluconazole levels may decrease with chronic coadministration of rifampin; coadministration of fluconazole may decrease phenytoin clearance; may increase concentrations of theophylline, tolbutamide, glyburide, and glipizide; effects of anticoagulants may increase with fluconazole coadministration; increases in cyclosporine concentrations may occur when administered concurrently |
| Pregnancy | C - Safety for use during pregnancy has not been established. |
| Precautions | Generally well tolerated, but approximately 12% of patients show adverse effects, which include nausea, vomiting, abdominal discomfort, and hepatotoxicity; adjust dose for renal insufficiency; monitor closely if rashes develop and discontinue drug if lesions progress; may cause clinical hepatitis, cholestasis and fulminant hepatic failure (including death), with underlying medical conditions (eg, AIDS or a malignancy) and while taking multiple concomitant medications; not recommended in breastfeeding |
| Media file 1: Inflammatory tinea barbae resulting from Trichophyton mentagrophytes var granulosum infection. | |
 | View Full Size Image | Media type: Photo |
| Media file 2: Wax model of kerionlike tinea barbae. Courtesy of the Museum of the Department of Dermatology, University of Medicine, Wroclaw, Poland. | |
 | View Full Size Image | Media type: Photo |
Article Last Updated: Feb 27, 2007
