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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; Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University; 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: tinea favosa, favus honeycomb ringworm, tinea favosa capitis

Background

Favus, also termed tinea favosa, is a chronic inflammatory dermatophytic infection usually caused by Trichophyton schoenleinii. Rarely, favus is caused by Trichophyton violaceum, Trichophyton mentagrophytes var quinckeanum, or Microsporum gypseum. Favus typically affects scalp hair but also may infect glabrous skin and nails. The causative agent of mouse favus is T mentagrophytes var quinckeanum, also termed Trichophyton quinckeanum, which can cause favus in humans, although rarely.

Pathophysiology

Favus is a superficial dermatophyte infection usually caused by T schoenleinii. In most patients, favus is a severe form of tinea capitis; however, it may occur, although rarely, as onychomycosis, tinea barbae, or tinea corporis.

Favus is 1 of 3 primary patterns of hair infection (ectothrix, endothrix, favus). Typically, hair is not as heavily infected as in trichophytosis caused by Trichophyton tonsurans. Hair is able to grow, and frequently, long hairs are observed in the disease state. The most characteristic feature is the formation of air spaces between hyphae within the infected hair. These air spaces (air tunnels) form as a result of autolysis of the hyphae. Arthroconidia rarely are seen within the hair. Such infected hair commonly is termed favus-type hair. In the sera of patients, antibodies to causative fungi are found by charcoal agglutination and immunodiffusion assay; however, the exact role of antibodies is not clear.

Frequency

United States

Favus is uncommon in the United States, although foci have been described in past decades in rural areas of West Virginia, New York, Kentucky, and Arkansas. Favus often is seen in geographic regions where lifestyles are associated with malnutrition, neglect, and poverty.

International

Foci have been seen worldwide, including Poland, Southern and Northern Africa, Pakistan, the United Kingdom, Australia, South America (Brazil), and the Middle East.

Mortality/Morbidity

Permanent alopecia with scarring often follows favus, which is a chronic disfiguring infection.

Race

Favus shows no racial or ethnic preference.

Sex

Both females and males may be affected equally; however, some report a slight predominance of female patients with favus.

Age

Favus appears in both children and adults. Favus usually is acquired during childhood or adolescence and typically persists into adulthood.



History

Favus usually begins on the scalp, often in childhood, and persists for many years as unsightly, crusted plaques. According to the severity of the disease, 3 main stages are described.

  • First stage: Only erythema of the scalp is seen, primarily around follicles. Hairs are not loose or broken.
  • Second stage: Formation of scutula is seen with the beginning of hair loss.
  • Third stage: The most severe stage involves large areas of the scalp (at least one third); extensive hair loss, atrophy, and scarring result. Formation of new scutula at the periphery of plaques is common.

Physical

The scutulum, a yellow cup-shaped crust that surrounds a hair and pierces its center, is characteristic. Scutula form a dense plaque, each composed of mycelia and epidermal debris. Often, a secondary bacterial infection occurs in the plaque. Plaque removal leaves an erythematous moist base. The dense masses of yellow crusts may be solitary or numerous, and in patients who are severely affected, involve the entire scalp. A mousy odor typically is present. Glabrous skin may show similar yellow crusting.

On glabrous skin, favus is a papulovesicular and papulosquamous eruption in which typical scutula may be evident. As an onychomycosis, tinea favosa resembles other forms of tinea unguium.

In addition to typical scutular favus on the scalp, several atypical manifestations of favus have been described.

  • Favus pityroides mimics dandruff or seborrheic dermatitis. Numerous small-to-large scales are present. On the surface, scales are loose; however, deeper layers are attached strongly to the base. Removal of scales uncovers reddish, moist, and scarring areas of skin.
  • Favus psoriasiformis is a psoriasis-imitating favus, both on the scalp and on glabrous skin. Instead of yellowish scutula, patients present with whitish scales mimicking the typical lesions of psoriasis.
  • Favus follicularis is characterized by cone-shaped wax-colored papules around the follicles. Hair shows the typical features of favus.
  • Favus impetigoides is characterized by yellowish (honey-colored) crusts imitating impetigo that are located on the scalp. Frequently, they form larger plaques that do not improve with antibacterial treatment. The characteristic mousy odor and dull hair suggest the diagnosis of favus.
  • Favus papyroides is characterized by small loci on the scalp that are covered by a brittle substance similar to parchment. Beneath, typical small scutula may be present.
  • Favus herpetiformis is an atypical variant of favus corporis. Round, erythematous, scaling plaques with small papules, vesicles, pustules, and/or crusts on the border are located on the trunk and extremities. This form of favus shows an annular shape and resembles the lesions typical of tinea corporis.

Causes

Primarily caused by T schoenleinii, favus rarely may be caused by T violaceum, T mentagrophytes var quinckeanum, or M gypseum. Although vertical transmission may occur, family attack rates are highly variable. Most evidence suggests that favus is not a highly contagious disease.



Candidiasis, Cutaneous
Folliculitis
Lupus Erythematosus, Discoid
Pseudopelade, Brocq
Psoriasis, Plaque
Seborrheic Dermatitis
Tinea Capitis

Other Problems to be Considered

Dissecting cellulitis
Lupus vulgaris
Pediculosis capitis
Pityriasis amiantacea
Systemic lupus erythematosus



Other Tests

  • Base the diagnosis on mycologic examination via direct microscopy and culture. Sporadically, the diagnosis can be confirmed by histologic evidence of fungal invasion of the hair. Wood lamp examination may demonstrate a dull green fluorescence.
  • Perform routine direct microscopic examination in 10-20% potassium hydroxide (KOH) solution, with or without dimethyl sulfoxide. This solution helps visualize fungal elements. With favus, hair must be examined immediately after adding KOH solution to observe the bubbling of KOH through the air spaces between hyphae elements. Examination of scutulum fragments shows segmental filaments and spores.
  • The causative organism is identified on culture, which usually is performed on Sabouraud agar with the addition of cycloheximide and chloramphenicol. These 2 substances inhibit growth of bacteria and other fungi; thus, pure dermatophyte colonies are obtained. In patients who are chronically affected, positive culture results may be difficult to obtain.

Histologic Findings

Hematoxylin and eosin staining may visualize fungal elements insufficiently; therefore, periodic acid-Schiff staining is recommended. Biopsy sections reveal mycelium in the scutulum and horny layer of the epidermis, which is atrophic. Scutulum borders show well-preserved hyphae; however, the center of the lesion contains degenerating mycelium and granular debris. A moderately severe inflammatory infiltrate is present in the dermis.



Medical Care

Although favus is not highly contagious, several family members may be affected, and all should be treated simultaneously. Treatment outcome depends on the stage at which the disease is arrested. Severe long-lasting disease can cause irreversible scarring alopecia.

In most patients, favus involves hair; therefore, the disease requires systemic treatment. Additional topical agents, such as shampoo (2% ketoconazole, 2.5% selenium sulfide), lotion, and cream may be helpful. X-ray epilation no longer is used. General hygiene of the scalp must be improved, and debris and crusts must be removed.

Favus usually is controlled by griseofulvin, the standard treatment of tinea capitis; however, a longer treatment course than usual for tinea capitis may be advisable. Currently, favus is uncommon; therefore, no clinical trials with newer antifungals are available. In vitro studies indicate that T schoenleinii is sensitive to newer antifungal drugs, similar to other dermatophytes. Terbinafine, itraconazole, and fluconazole in a similar dosage schedule to tinea capitis may eradicate the fungus and cure the disease.



The goals of pharmacotherapy are to eradicate the infection, to reduce morbidity, and to prevent complications.

Drug Category: Antifungals

Mechanism of action usually involves inhibiting pathways (enzymes, substrates, transport) necessary for sterol/cell membrane synthesis or altering the permeability of the cell membrane (polyenes) of the fungal cell.

Drug NameGriseofulvin (Fulvicin P/G, Grifulvin V)
DescriptionFungistatic activity. Dermatophytes are sensitive, but yeastlike fungi and molds are resistant. 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 Dose500 mg microsize (330-375 mg ultramicrosize) PO divided bid
Pediatric Dose20-25 mg microsize/kg/d PO divided bid or
15 mg ultramicrosize/kg/d PO divided bid
ContraindicationsDocumented hypersensitivity; hepatic injury
InteractionsReduced effects of cyclosporine, salicylates, and warfarin (decreased hypoprothrombinemic activity); contraceptives may lose their effectiveness; avoid alcohol use (disulfiramlike reaction may occur); intense UV light exposure may cause phototoxic reaction
PregnancyC - Safety for use during pregnancy has not been established.
PrecautionsOn prolonged therapy, observe patients closely; monitor renal, hepatic, and hematopoietic function regularly; Lupus-like syndromes or exacerbation of lupus erythematosus may occur; photosensitivity may also occur and thus patients should take protective measures against exposure to ultraviolet light or sunlight; take with or just after fatty food (increases absorption); reported adverse effects most commonly include abdominal pain, nausea, diarrhea, and headache

Drug NameTerbinafine (Lamisil)
DescriptionFungicidal agent and member of allylamine family.
Inhibits squalene epoxidase, which decreases ergosterol synthesis, causing fungal-cell death.
Use until symptoms significantly improve.
In young children, tab may be split and hidden in food.
Adult Dose250 mg/d PO for minimum of 4 wk; not to exceed 12 wk
Pediatric Dose<2 years (usually <12 kg): Not established
<20 kg: 62.5 mg/d PO single dose
21-40 kg: 125 mg/d PO single dose
>40 kg: 250 mg/d PO single dose
ContraindicationsDocumented hypersensitivity
InteractionsMay decrease cyclosporine effects; toxicity of terbinafine may increase with rifampin and cimetidine
PregnancyB - Usually safe but benefits must outweigh the risks.
PrecautionsDiscontinue use if chemical irritation develops with topical use or if hepatobiliary dysfunction, neutropenia, or Stevens-Johnson syndrome develops; changes in the ocular lens and retina reported; in controlled trials; clinical significance of this unknown; generally well tolerated but approximately 10.5% of patients show adverse effects, primarily GI; transient loss of sense of taste is rare but specific adverse effect

Drug NameItraconazole (Sporanox)
DescriptionFungistatic 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.
Not registered for administration in children in most countries.
Adult Dose400 mg/d PO divided bid for 1 wk or 200 mg/d PO divided bid for 4 wk
Pediatric Dose<20 kg: 3-5 mg/kg/d PO divided bid
>20 kg: 100 PO single dose or 200 mg/d PO divided bid
ContraindicationsCoadministration of terfenadine, astemizole, or cisapride with Sporanox (itraconazole cap); concomitant administration with oral triazolam or with oral midazolam; administration for the treatment of onychomycosis to pregnant patients or to women contemplating pregnancy
InteractionsFrequent: Increased level of cyclosporine, tacrolimus, and digoxin may occur after coadministration; phenytoin and rifampin may decrease itraconazole effect; amlodipine and nifedipine taken with itraconazole 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)
PregnancyC - Safety for use during pregnancy has not been established.
PrecautionsCaution in hepatic insufficiencies; generally well tolerated, but approximately 12% of patients show adverse effects, which primarily include GI abnormalities; hepatobiliary dysfunction was observed; take with fatty food, which increases absorption in alimentary tract

Drug NameFluconazole (Diflucan)
DescriptionFungistatic 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 Dose150 mg PO qwk for approximately 6 wk
Pediatric Dose<6 months: Not established
>6 months: 5-6 mg/kg/d PO for 4-6 wk (liquid or tab)
ContraindicationsDocumented hypersensitivity
InteractionsLevels may increase with thiazides; 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
PregnancyC - Safety for use during pregnancy has not been established.
PrecautionsAdjust dose in 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 such as AIDS or a malignancy and while taking multiple concomitant medications; not recommended for breastfeeding; convenience and efficacy of single dose regimen for treatment of vaginal yeast infections should be weighed against difficulties resulting from higher incidence of adverse reactions reported with oral fluconazole versus intravaginal agents; generally well tolerated, but approximately 12% of patients show adverse effects, which primarily include nausea, vomiting, abdominal discomfort, and hepatotoxicity



Further Outpatient Care

  • Monitor patients and their families for favus in regions where lifestyles are associated with malnutrition, neglect, and poverty.

Deterrence/Prevention

  • Breaking the lifestyle chain associated with malnutrition, neglect, and poverty can prevent this infection and possibly deter recurrence.

Prognosis

  • Favus shows no tendency to resolve spontaneously.
  • Cicatricial alopecia with skin atrophy is a common feature of long-lasting disease. In these patients, both scalp and glabrous skin often are affected.



Medical/Legal Pitfalls

  • Failure to recognize and treat favus adequately may present a potential for litigation, since untreated favus may result in scarring alopecia. Preventable permanent cosmetic disfigurement may occur.



Media file 1:  Tinea favosa of the scalp shows erythematous lesions with pityroid scaling. Some hairs are short and brittle.
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Media file 2:  Favus of the scalp shows extensive lesions with scarring alopecia.
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Media file 3:  Typical fluorescence under Wood lamp examination.
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Media file 4:  Favus, wax montage. Courtesy of Professor Dr Feliks Wasik, Dermatology, Medical University of Wroclaw, Poland.
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Media file 5:  Black man, aged 45 years, with favuslike yellow crusting of scalp. Potassium hydroxide and fungal culture were negative.
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Media file 6:  Culture of Trichophyton schoenleinii on Sabouraud agar. Courtesy of Anna Pawlowicz, PhD, and Professor Barbara Raszeja-Kotelba, MD, Dermatology, University School of Poznan, Poland.
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Media type:  CT

Media file 7:  Culture of Trichophyton schoenleinii on Sabouraud agar. Note pleomorphism of the culture. Courtesy of Anna Pawlowicz, PhD, and Professor Barbara Raszeja-Kotelba, MD, Dermatology, University School of Poznan, Poland.
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Media type:  Photo

Media file 8:  Microculture of Trichophyton schoenleinii shows dichotomic branching and terminal swelling. Light-field microscopy, original magnification X 1000. Courtesy of Anna Pawlowicz, PhD, and Professor Barbara Raszeja-Kotelba, MD, Dermatology, University School of Poznan, Poland.
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Media type:  Photo

Media file 9:  Microculture of Trichophyton schoenleinii shows characteristic dichotomic branching. Light-field microscopy, original magnification X 1000. Courtesy of Anna Pawlowicz, PhD, and Professor Barbara Raszeja-Kotelba, MD, Dermatology, University School of Poznan, Poland.
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Media type:  Photo

Media file 10:  Microculture of Trichophyton schoenleinii shows numerous terminal chlamydospores. Light-field microscopy, original magnification X 1200. Courtesy of Anna Pawlowicz, PhD, and Professor Barbara Raszeja-Kotelba, MD, Dermatology, University School of Poznan, Poland.
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Media file 11:  Infected hair filled with hyphae shows bubbles of gas and gas tunnels (light field microscopy, original magnification X 2300).
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Media type:  Photo



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Favus excerpt

Article Last Updated: Feb 26, 2007