Favus - Symptoms, Diagnosis, and Treatment

Favus (tinea favosa) is a chronic form of dermatophytosis of the scalp, primarily caused by the anthropophilic fungus Trichophyton schoenleinii. The classic symptom is "scutulae": gray-yellow, cup-shaped crusts around the hair shaft with a characteristic "mousy" odor that eventually coalesce into plaques. Without treatment, the process lasts for years and ends with skin atrophy and persistent cicatricial alopecia in the affected areas. Less commonly, favus affects smooth skin, the beard, and nails. [1]

Today, favus occurs sporadically in developed countries, but outbreaks persist in regions with overcrowding, poverty, and limited access to dermatological care. Cases have been described in the Middle East, North and South Africa, Pakistan, Brazil, Poland, and the United Kingdom. In some patients, the infection begins in childhood and can persist into adulthood. The disease is moderately contagious: intrafamilial cases are common in closely-knit families. [2]

Pathogenetically, T. schoenleinii forms foci of mycelium at the base of the hair and air spaces in the hair shaft ("favic hair"), which distinguishes favus from other variants of scalp ringworm. This explains the chronic course with a minimal inflammatory reaction, but a high probability of scarring with prolonged persistence of the lesion. [3]

The key to a favorable outcome is early systemic treatment (oral antifungals) and family anti-epidemic measures. Topical treatments alone are ineffective for hair lesions; their role is adjuvant. [4]

Code according to ICD-10 and ICD-11

In ICD-10, favus of the head is coded in block B35 “Dermatophytosis”; lesions of the scalp and beard - B35.0, nails - B35.1, smooth skin - B35.4; the term “favus” itself is included in the substantive description of section B35. [5]

In ICD-11, dermatophytosis is grouped into block 1F28. For scalp favus, 1F28.0 "Dermatophytosis of scalp" is used; for nail favus, 1F28.1 is used; for other localizations, the corresponding subheadings are used (e.g., 1F28.Y "Other specified dermatophytosis"). The current version is MMS v2025-01. [6]

Table 1. Correspondence of codes for favus by localization

Localization	ICD-10	ICD-11
Scalp (tinea capitis, favus)	B35.0	1F28.0
Beard (tinea barbae, favus barbae)	B35.0	1F28.Y (to be specified by post-coordination)
Smooth skin (tinea corporis favosa)	B35.4	1F28.Y
Nails (onychomycosis favosa)	B35.1	1F28.1
Note: specification/post-coordination by pathogen and form is possible in ICD-11. [7]

Epidemiology

Favus is a rare form of tinea capitis in countries with high access to treatment; foci persist in regions with low socioeconomic status and crowded living conditions. Familial cases and long-term persistence from childhood have been described. Precise prevalence rates for favus by country are currently limited, reflecting the true rarity and lack of registration. [8]

In adults, the proportion of cases of tinea capitis, according to various estimates, is 3-11%; however, the proportion of favus within this sample is small and geographically variable. Population movement and the availability of systemic antifungal agents have significantly reduced classic favus outbreaks, but imported and familial clusters do occur. [9]

In tinea capitis, the leading pathogens generally depend on the region (in Northern Europe and New Zealand, most often Microsporum canis, in the USA, Trichophyton tonsurans ), whereas favus is typically associated with T. schoenleinii. [10]

Table 2. Epidemiological emphasis on favus

Indicator	What is known today
Status	Rare, focal, familial clusters
Typical age of onset	Childhood/adolescence, often persists into adulthood
Geography	Hotspots: Middle East, Africa, South Asia, parts of Europe/Latin America
Contagiousness	Moderate; role of close contact and fomites is significant
[11]

Reasons

The main cause is infection with the anthropophilic dermatophyte Trichophyton schoenleinii. In rare reports, "favus-like" pictures have been described with other dermatophytes (including Microsporum spp.), but classical favus is almost always associated with T. schoenleinii.[12]

Transmission routes include direct hair-to-hair/skin-to-skin contact and through fomites (combs, hats, pillows, towels). Spores can persist on objects for months, supporting intrafamilial circulation. [13]

Risk factors

Key factors include crowded living conditions, poor hygiene, chronic colonization within the family, and prolonged lack of treatment. Immunodeficiencies and concomitant scalp dermatoses increase the risk of atypical and disseminated disease. Contact with contaminated objects is an independent factor, especially in children's groups. [14]

Table 3. Factors supporting favus in foci

Factor	Mechanism
Overcrowding/poverty	Increased household contacts and shared fomites
Low availability of dermatological care	Late diagnosis, chronic course
Familial carriers/untreated cases	Constant reinfection
Immune disorders	Severe/atypical forms
[15]

Pathogenesis

In favus, the fungus forms clusters of hyphae at the follicle opening and within the hair shaft. Prolonged presence of scutulae leads to follicular dystrophy and dermal atrophy in the affected area, resulting in cicatricial alopecia. Unlike acute zoophilic forms (kerion), active purulent inflammation is usually absent, masking the severity of the process until its later stages. [16]

Trichoscopic examination of scalp dermatophytosis generally reveals "comma-shaped," "corkscrew-shaped," "zigzag," and "morse-code" hairs; in favus, dense crusts and massive focal scales are additionally visualized. These findings facilitate initiation of treatment before cultures are ready. [17]

Symptoms

There is usually no prodrome. It begins with a small erythema around the follicles, followed by the formation of gray-yellow cup-shaped scabs surrounding the hair shaft: the hair becomes matted, thins, and begins to fall out. Affected areas may emit a "mousy" odor; when the scabs are removed, a moist, hyperemic surface is revealed. With prolonged progression, skin atrophy and persistent cicatricial alopecia develop over a large area. [18]

Outside the scalp, lesions may occur on the beard, smooth skin, and nails; however, the clinical presentation is less specific, and diagnosis is often delayed. Secondary bacterial colonization of the scutulae is common and exacerbates the inflammation. [19]

Table 4. Stages of favus (clinical)

Stage	What is visible	Comment
I	Erythema of the follicle orifices, hair is preserved	The beginning of the process
II	Scutulas, hair loss	The "mouse" smell is not uncommon
III	Wide plaques of scutula, atrophy, scars	Irreversible alopecia
[20]

Classification, forms and stages

In addition to the typical scalp favus, clinical subtypes have been described: favus pityroides (pseudo-seborrheic pattern), favus psoriasiformis (psoriasiform), favus follicularis, favus impetigoides, favus papyroides, favus herpetiformis (lesions on the trunk/limbs). These variants complicate clinical diagnosis and require mycological confirmation. [21]

The stages (I-III) correspond to the increase in area, thickness of the crusts, and depth of damage to the follicles before scarring. In a practical sense, when planning therapy, it is important to distinguish between localized favus, spread over several zones, and complicated favus (secondary bacterial infection). [22]

Complications and consequences

The main late consequence is irreversible cicatricial alopecia with significant psychoemotional impact. Frequent accompanying problems include secondary bacterial infection within the scutella and regional lymphadenitis. If the infection remains untreated for a long time, it may involve the eyebrows/eyelashes, resulting in aesthetically significant defects. Rarely, painful erosions may form after removal of massive crusts. [23]

When to see a doctor

Immediately - if the rash in a child rapidly expands, painful, purulent crusts, or signs of phlegmonous inflammation appear. Urgently - if hair loss occurs alongside yellow crusts, a "mousy" odor, and/or there is a family history of similar rashes. Scheduled, but urgently - for any chronic flaking of the scalp that is resistant to shampoos, especially in close quarters. Adults with lesions that appeared in childhood should be tested for carrier status and have their surroundings cleaned. [24]

Diagnostics

1. Clinical examination + trichoscopy. Examination reveals cuticles; trichoscopy reveals characteristic dermatophyte signs (comma/corkscrew/morse-code hairs, etc.), which supports early initiation of systemic therapy before culture. [25]
2. Wood's lamp. T. schoenleinii typically produces a dull bluish-greenish fluorescence in hairs; most other Trichophyton species do not fluoresce, but Microsporum often produces a bright green fluorescence, which helps select hairs for analysis. [26]
3. KOH microscopy. Rapid verification of hyphae/arthroconidia in plucked hairs/scutulae. Provides answers within hours and guides therapy. [27]
4. Culture and/or PCR. Culture confirms the species (including T. schoenleinii ), but is slow (up to 4 weeks); PCR is faster and more sensitive where available. A scalp biopsy is useful if the presentation is atypical. [28]

Table 5. Diagnostic clues

Method	What are we looking for?	For what
Trichoscopy	"Comma", "corkscrew", "Morse-code" hair	Rapid confirmation of dermatophytosis
Wood's lamp	Dull blue glow ( T. schoenleinii ) / bright green ( Microsporum )	Selection of hair for KOH/seeding
KOH microscopy	Hyphae/arthroconidia	Quick verification
Sowing/PCR	Species identification	Targeted drug selection/epidemiological control
[29]

Differential diagnosis

Seborrheic dermatitis and scalp psoriasis mimic scaling without scutulae and with a lesser degree of alopecia. Alopecia areata and trichotillomania cause focal hair loss without a pronounced scaly crust. Discoid lupus erythematosus and lichen planopilaris result in cicatricial plaques, but mycology is negative; impetigo and pyoderma produce honey-like crusts, often painful and with positive bacterial cultures. In children, it is important to distinguish from kerion (an acute inflammatory, usually zoophilic form with a risk of scarring), where the management differs. [30]

Table 6. How favus differs from “similar” conditions

State	Key feature	Test-solver
Seborrheic dermatitis	Diffuse dandruff without scutulas	KOH/culture negative, Wood's lamp negative.
Psoriasis	Erythematous plaques with silvery scales	Mycology negative.
Alopecia areata	"Clean" areas of hair loss	Mycology is negative, trichoscopy is autoimmune
Impetigo	Honey-like crusts, pain	Bacterial culture +
Kerion	Acute painful infiltration, pus	Inflammation ↑, often Microsporum, treatment other
[31]

Treatment

Basic principle. Hair lesions require systemic therapy: no shampoo penetrates the hair matrix in an effective concentration. Treatment can be initiated after clinical and trichoscopic suspicion, without waiting for culture. The goal is to eradicate the fungus, prevent scarring, and stop intrafamilial transmission. Effectiveness is monitored clinically and mycologically. [32]

Griseofulvin. A classic drug for tinea capitis, including favus, with proven efficacy against anthropophilic dermatophytes. Recommended doses: micronized griseofulvin 20-25 mg/kg/day (or ultramicronized 10-15 mg/kg/day) for 6-12 weeks, continuing for 2 weeks after clinical recovery. The drug is well tolerated, laboratory monitoring is usually not necessary; it is contraindicated in pregnancy and severe hepatopathies. Availability varies by country. [33]

Terbinafine. A fungicidal drug with excellent penetration into follicles; for Trichophyton infections, efficacy is comparable to or superior to griseofulvin in shorter courses. Dosage in children is by weight (125/187.5/250 mg), in adults it is often 250 mg/day; courses are 4-6 weeks (sometimes 2 weeks for Trichophyton according to small studies). For courses >6 weeks, monitoring of liver enzymes is appropriate. Terbinafine is less effective against Microsporum, but works well against T. schoenleinii. [34]

Itraconazole and fluconazole. These are alternatives/step therapy in cases of intolerance or unavailability of first-line therapies. Itraconazole is used continuously or in pulsed regimens (in children, doses based on weight; in adults, often 200 mg/day), with ALT/AST monitoring due to rare but possible drug-induced hepatitis and drug interactions. Fluconazole (in children, ≈6 mg/kg/day; in adults, 150-300 mg/week) is used for 3-6 weeks. The choice depends on the pathogen, comorbidities, and drug interactions. [35]

What to choose for T. schoenleinii. In cases of confirmed Trichophyton (including T. schoenleinii ), modern reviews accept terbinafine as an equivalent or preferred alternative to griseofulvin in terms of efficacy and ease of administration; if griseofulvin is unavailable, it is a working choice. Itraconazole is also effective against Trichophyton. For Microsporum (if culture/Wood's lamp indicates it), it is more logical to return to griseofulvin. [36]

Topical treatments are a complementary treatment. Shampoos containing 2% ketoconazole or 2.5% selenium sulfide are used 2-3 times a week to reduce spore burden (patient and close family contacts). Regular softening and gentle removal of crusts improves drug penetration and lesion hygiene. Ointments/creams play a secondary role and are not a substitute for systemic treatment. [37]

Environmental sanitation. All family members must be tested (asymptomatic carriers may exist) and treated with shampoos if dermatophytosis is detected. Avoid sharing combs, hats, and pillowcases; fomites are washed and treated, as spores can persist on surfaces for months. Pets are examined only if a zoophilic source is suspected (not typical for favus). [38]

Treatment of complications. If a bacterial infection occurs, local antiseptics/antibacterial agents are used as indicated. In cases of severe pain and swelling (if the picture shifts to the kerion), in exceptional situations, briefly add systemic glucocorticosteroids under the supervision of a dermatologist; for classic favus, this is not routine. Unfortunately, scars do not restore hair; camouflage/trichopigmentation are discussed, and less commonly, transplantation after stable remission. [39]

Monitoring of cure. Clinical features (disappearance of cutulae, cessation of hair breakage, disappearance of odor) and, if possible, mycological examination (repeat KOH/culture) are assessed. In case of relapse, compliance with sanitary measures, adequacy of dosage/duration, and sources of reinfection are checked. Remember: late initiation of treatment is the main predictor of scarring. [40]

Adult patients. The principles are the same as for children: systemic medication + environmental sanitation. A modern review of tinea capitis in adults recommends the same molecules (griseofulvin/terbinafine/itraconazole/fluconazole) with dose adjustments and consideration of drug interactions; follow-up after approximately 1 month from initiation is a reasonable standard. [41]

Table 7. Systemic therapy for favus (approximate)

Preparation	Dosage and course (typical)	Notes
Griseofulvin	20-25 mg/kg/day (micronized), 6-12 weeks; +2 weeks after clinical remission	Effective; availability varies by country
Terbinafine	Children: 125/187.5/250 mg by weight; adults: 250 mg/day, 4-6 weeks	Good for Trichophyton, including T. schoenleinii
Itraconazole	By weight in children; adults often 200 mg/day, 2-4 weeks (or pulses)	Monitoring of liver enzymes is necessary.
Fluconazole	Children ≈6 mg/kg/day; adults 150-300 mg/week, 3-6 weeks	Alternative in case of intolerance/availability
[42]

Table 8. The role of local and organizational measures

Measure	To whom	For what
Ketoconazole/selenium sulfide shampoos	Patient + family	Reduce sporulation
Removing crusts	Patient	Improve access to drugs
No shared combs/hats	All in the family	Break the spore circulation
Inspection of contacts	All in the family	Identify carriers/treat synchronously
[43]

Prevention

Prevention is based on early recognition and treatment of isolated cases, family sanitation, and avoiding the sharing of hair care items. In outbreaks, education of parents and staff at childcare facilities and prompt access to systemic therapy are essential. Animals should be examined if there is contact with cats or dogs in the family and a zoophilic dermatophyte is suspected (usually not relevant for T. schoenleinii ). Using antifungal shampoos in contacts for several weeks reduces the risk of colonization. [44]

Forecast

With early initiation of systemic therapy, the prognosis is good: complete eradication of the pathogen and cessation of hair loss are possible. With late treatment and prolonged persistence of cutulae, there is a high risk of cicatricial alopecia, which is irreversible. Relapses are most often associated with poor sanitary measures and unsanitary contact. Monitoring the effectiveness of treatment and short-term observation after treatment are warranted. [45]

FAQ

Is Favus contagious? Yes, moderately; it is transmitted through close contact and through fomites (combs, hats, pillows). Handle/wash items separately and do not share them. [46]

Will "shampoo alone" help? No. Hair lesions require systemic therapy; shampoos are merely a supplement to reduce sporulation. [47]

How to recognize it at home? Yellow "cups" around the hair ("scutulae"), dull, brittle hair, a specific odor; but the diagnosis must be confirmed by a doctor (KOH/culture/Wood's lamp/trichoscopy). [48]

What dose and how much should be taken? Depends on the drug and age: griseofulvin 6-12 weeks, terbinafine 4-6 weeks, etc.; the exact regimen is determined by the doctor, taking into account the pathogen and concomitant diseases. [49]

What if it's not T. schoenleinii? For Microsporum, griseofulvin is preferred; a Wood's lamp and culture help to avoid making a mistake in choosing. [50]