Tinea favosa, often called Favus, is a severe, long-term fungal infection that primarily targets the scalp. It is recognized as the most damaging form of tinea capitis, or ringworm of the scalp. The condition is characterized by its chronic nature and potential for deep, permanent tissue damage. While once a widespread global issue, improvements in public health and effective treatments have made it exceptionally rare in most modern developed countries.
Unique Clinical Presentation of Tinea Favosa
The most distinctive physical sign of Tinea Favosa is the development of sulfur-yellow, cup-shaped crusts known as scutula. These formations typically grow around the base of the hair follicles. Scutula are considered pathognomonic, meaning their presence is highly specific to this infection. They are composed of a dense accumulation of fungal filaments, hair fragments, and epithelial cells, often coalescing to form thick, honeycomb-like plaques on the scalp.
The growth of these crusts exerts pressure on the underlying skin and hair structures, leading to chronic inflammation and subsequent atrophy. This sustained damage often results in permanent, scarring alopecia, where the hair follicles are entirely destroyed and replaced by scar tissue. The hair loss associated with Tinea Favosa is typically irreversible, even after the infection is cleared.
A notable feature accompanying advanced infection is a distinct, unpleasant “mousy” or “cheesy” odor emanating from the affected scalp. This smell is caused by metabolic byproducts released by the fungus within the crusts. The infection can persist for many years, often starting in childhood and continuing untreated into adulthood, resulting in a combination of crusts, inflamed skin, and bald, scarred patches.
Etiology and Global Distribution
Tinea Favosa is caused by the dermatophyte fungus Trichophyton schoenleinii, which is responsible for the vast majority of documented cases. This fungus is classified as anthropophilic, meaning its primary host is the human population, and it is usually transmitted directly between people. Transmission often occurs through close contact within families or shared use of contaminated items such as hats, combs, or bedding.
T. schoenleinii is highly adapted to human skin and hair, contributing to the chronic nature of the infection. While other Trichophyton species can occasionally cause a favus-like presentation, the classic, severe form is linked to this specific pathogen. The fungus invades the hair shaft through a pattern known as endothrix infection, where the fungal elements fill the inside of the hair.
Historically, Tinea Favosa was common worldwide, particularly in areas with poor hygiene, malnutrition, and overcrowding. Following public health improvements and the introduction of effective systemic antifungal drugs, the incidence has dramatically declined in Western nations. Today, the infection is largely confined to specific endemic pockets, primarily found in parts of Eastern Europe, the Middle East, Africa, and Central Asia.
Diagnosis and Treatment Protocols
The diagnostic process begins with a clinical examination to identify the characteristic scutula and scarring alopecia, which immediately suggest the condition. Physicians may use a Wood’s lamp, an ultraviolet light source, to examine the affected areas. Infected hairs often fluoresce a dull green under the lamp, though this finding is not always consistent.
To confirm the presence of the fungus, microscopic examination of hair and crust samples is performed using a potassium hydroxide (KOH) preparation. This test dissolves the keratin, making the fungal hyphae and spores within the hair shaft visible. The definitive diagnosis relies on fungal culture, where the collected material is grown in a laboratory on a specialized medium, such as Sabouraud dextrose agar, to isolate and identify Trichophyton schoenleinii.
Because the fungus invades deep into the hair shaft, Tinea Favosa requires systemic antifungal therapy, as topical treatments alone are ineffective. The standard treatment for many years was oral griseofulvin, often administered for several months. Newer systemic antifungals, such as terbinafine or itraconazole, are also used and may offer a shorter treatment duration.
Systemic medication is supplemented with supportive care measures to enhance treatment efficacy and hygiene. These measures include the manual removal of the scutula crusts and the regular use of medicated shampoos containing agents like ketoconazole or selenium sulfide. Treatment must be sustained until mycological cure is confirmed by repeated negative fungal cultures, as stopping medication prematurely can lead to recurrence and further scarring.