eMedicine Specialties > Dermatology > Fungal Infections

Tinea Capitis

Author: Grace F Kao, MD, Clinical Professor of Dermatopathology, Department of Dermatology, George Washington University Medical School; Director of Dermatopathology, Department of Pathology and Laboratory Medicine, Veterans Affairs Maryland Healthcare System
Contributor Information and Disclosures

Updated: Jan 17, 2008

Introduction

Background

Tinea capitis is a disease caused by superficial fungal infection of the skin of the scalp, eyebrows, and eyelashes, with a propensity for attacking hair shafts and follicles. The disease is considered to be a form of superficial mycosis or dermatophytosis. Several synonyms are used, including ringworm of the scalp and tinea tonsurans. In the United States and other regions of the world, the incidence of tinea capitis is increasing.

Dermatophytosis includes several distinct clinical entities, depending on the anatomic site and etiologic agents involved. Clinically, the conditions include tinea capitis, tinea favosa (favus resulting from infection by Trichophyton schoenleinii), tinea corporis (ringworm of glabrous skin), tinea imbricata (ringworm resulting from infection by Trichophyton concentricum), tinea cruris (ringworm of the groin), tinea unguium or onychomycosis (ringworm of the nail), tinea pedis (ringworm of the feet), tinea barbae (ringworm of the beard), and tinea manuum (ringworm of the hand).

Clinical presentation of tinea capitis varies from a scaly noninflamed dermatosis resembling seborrheic dermatitis to an inflammatory disease with scaly erythematous lesions and hair loss or alopecia that may progress to severely inflamed deep abscesses termed kerion, with the potential for scarring and permanent alopecia. The type of disease elicited depends on interaction between the host and the etiologic agents.

The term tinea originally indicated larvae of insects that fed on clothes and books. Subsequently, it meant parasitic infestation of the skin. By the mid 16th century, the term was used to describe diseases of the hairy scalp. The term ringworm referred to skin diseases that assumed a ring form, including tinea. The causative agents of tinea infections of the beard and scalp were described first by Remak and Schönlein, then by Gruby, during the 1830s. Approximately 50 years later, in Sabouraud's dissertation, the endothrix type of tinea capitis infection was demonstrated, and it was known that multiple species of fungi cause the disease. Simple culture methods were described and treatment using x-ray epilation was reported in 1904. Effective treatment of tinea capitis by griseofulvin became available in the 1950s.

Pathophysiology

Tinea capitis is caused by fungi of species of genera Trichophyton and Microsporum. Tinea capitis is the most common pediatric dermatophyte infection worldwide. The age predilection is believed to result from the presence of Pityrosporum orbiculare (Pityrosporum ovale), which is part of normal flora, and from the fungistatic properties of fatty acids of short and medium chains in postpubertal sebum.

Causative agents of tinea capitis include keratinophilic fungi termed dermatophytes. These molds usually are present in nonliving cornified layers of skin and its appendages and sometimes are capable of invading the outermost layer of skin, stratum corneum, or other keratinized skin appendages derived from epidermis, such as hair and nails.

Dermatophytes cause a variety of clinical conditions. They are among the most common infectious agents of humans. Collectively, the group of diseases is termed dermatophytosis. From the site of inoculation, the fungal hyphae grow centrifugally in the stratum corneum. The fungus continues downward growth into the hair, invading keratin as it is formed. The zone of involvement extends upwards at the rate at which hair grows, and it is visible above the skin surface by days 12-14. Infected hairs are brittle, and by the third week, broken hairs are evident.

The infection continues (for 8-10 wk) to spread in the stratum corneum to involve other hairs, at which point, the infected area is approximately 3.5-7.0 cm in diameter. The spontaneous cure of naturally occurring infection at puberty is a familiar clinical observation; however, the precise mechanism is unclear.

Three types of in vivo hair invasion are recognized.

• Ectothrix invasion is characterized by the development of arthroconidia on the exterior of the hair shaft. The cuticle of the hair is destroyed, and infected hairs usually fluoresce a bright greenish-yellow color under a Wood lamp ultraviolet light. Common agents include Microsporum canis, Microsporum gypseum, Trichophyton equinum, and Trichophyton verrucosum.
• Endothrix hair invasion is characterized by the development of arthroconidia within the hair shaft only. The cuticle of the hair remains intact and infected hairs do not fluoresce under a Wood lamp ultraviolet light. All endothrix-producing agents are anthropophilic (eg, Trichophyton tonsurans, Trichophyton violaceum).
• Favus, usually caused by T schoenleinii, produces favuslike crusts or scutula and corresponding hair loss.

Frequency

United States

Occurrence of the disease is no longer registered by public health agencies; therefore, true incidence is unknown. The reported peak incidence occurs in school-aged African American male children.

Tinea capitis is predominantly a disease of preadolescent children. It accounts for up to 92.5% of dermatophytoses in children younger than 10 years. The disease is rare in adults, although occasionally, it may be found in elderly patients. Tinea capitis occurrence is widespread in some urban areas in the United States.

International

Tinea capitis is widespread in some urban areas, particularly in children of Afro-Caribbean extraction, in North America, Central America, and South America. It is common in parts of Africa and India. In Southeast Asia, the rate of infection has been reported to have decreased dramatically from 14% (average of male and female children) to 1.2% in the last 50 years because of improved general sanitary conditions and personal hygiene. In northern Europe, the disease is sporadic.

In the United Kingdom and North America, T tonsurans accounts for greater than 90% of cases of infection . In the nonurban communities, sporadic infections acquired from puppies and kittens are due to M canis, which accounts for less than 10% of cases in the United Kingdom. Occasional infection from other animal hosts (eg, T verrucosum from cattle) occur in rural areas.

Mortality/Morbidity

Classification and severity of tinea capitis depend on the site of formation of their arthroconidia.

• Ectothrix infection is defined as fragmentation of the mycelium into conidia around the hair shaft or just beneath the cuticle of the hair, with destruction of the cuticle. Inflammatory tinea related to exposure to a kitten or puppy usually is a fluorescent small spore ectothrix. Some mild ringworm or prepubertal tinea capitis infections are of the ectothrix type, also termed the gray-patch type (microsporosis; see Media File 1). Some ectothrix infections involute during the normal course of disease without treatment. Depending on the extent of associated inflammation, lesions may heal with scarring.
• Endothrix infections are noted in which arthrospores are present within the hair shaft in both anagen and telogen phases, contributing to the chronicity of the infections. Endothrix infections tend to progress, become chronic, and may last into adult life. Lesions can be eradicated by systemic antifungal treatment. Since the organisms usually remain superficial, little potential for mortality exists. Disseminated systemic disease has been reported in patients who are severely immunocompromised.

Sex

Incidence of tinea capitis may vary by sex, depending on the causative fungal organism. In Microsporum audouinii –related tinea capitis, boys are affected much more commonly. The infection rate has been reported to be up to 5 times higher in boys than in girls; however, the reverse is true after puberty, possibly as a result of increased exposure to infected children by women and to hormonal factors. In infection by M canis, the ratio varies, and the infection rate usually is higher in male children. Girls and boys are affected equally by Trichophyton infections of the scalp, but in adults, women are infected more frequently than are men.

Age

Tinea capitis occurs primarily in children and occasionally in other age groups. It is seen most commonly in children younger than 10 years. Peak age range is in patients aged 3-7 years.

Clinical

History

• Infection begins as a small erythematous papule around a hair shaft on the scalp, eyebrows, or eyelashes.
• Within a few days, the red papule becomes paler and scaly, and the hairs appear discolored, lusterless, and brittle. They break off a few millimeters above the scalp skin surface.
• The lesion spreads, forming numerous papules in a typical ring form (see Media File 1). Ring-formed lesions may coalesce with other infected areas.
• Pruritus usually is minimal but may be intense at times.
• Alopecia is common in infected areas.
• Inflammation may be mild or severe. Deep boggy red areas characterized by a severe acute inflammatory infiltrate with pustule formation are termed kerions or kerion celsi (see Media File 2).
• Favus (also termed tinea favosa) is a severe form of tinea capitis.
  • Favus is a chronic infection and is caused most commonly by T schoenleinii and, occasionally, by T violaceum or Microsporum gypsum.
  • Scalp lesions are characterized by the presence of yellow cup-shaped crusts termed scutula, which surround the infected hair follicles.
  • Favus is seen predominantly in Africa, the Mediterranean, and the Middle East and, rarely, in North America and South America, usually in descendants of immigrants from endemic areas.
  • Favus usually is acquired early in life and has a tendency to cluster in families.
• In favus, infected hairs appear yellow.

Physical

A variety of clinical presentations of tinea capitis are recognized as being inflammatory or noninflammatory and are usually associated with patchy alopecia. However, the infection may be widespread, and the clinical appearances can be subtle. In urban areas, tinea capitis should be considered in the differential diagnosis of children older than 3 months with a scaly scalp until proven negative by mycological examination. Infection may also be associated with painful regional lymphadenopathy, especially in the inflammatory variants.
 
Pertinent physical findings are limited to the skin of scalp, eyebrows, and eyelashes.

• Primary skin lesions
  • Lesions begin as red papules with progression to grayish ring-formed patches containing perifollicular papules.
  • Pustules with inflamed crusts, exudate, matted infected hairs, and debris may be seen.
  • Black dot tinea capitis refers to an infection with fracture of the hair, leaving the infected dark stubs visible in the follicular orifices.
  • Kerion celsi may progress to a patchy or diffuse distribution and to severe hair loss with scarring alopecia (see Media File 3).
• Id reaction: Dermatophyte idiosyncratic or id reactions are manifestations of the immune response to dermatophytosis.
  • Id reactions occur at a distant site, and the lesions are devoid of organisms.
  • Id reactions may be triggered by antifungal treatment.
  • The most common type of id reaction is an acute vesicular dermatitis of the hands and feet. The grouped vesicles are tense, pruritic, and sometimes painful. Id reactions are noted in patients with inflammatory ringworm of the feet, primarily resulting from infection by Trichophyton mentagrophytes. Similar lesions may occur on the trunk in tinea capitis.
  • Vesicular lesions may evolve into a scaly eczematoid reaction or a follicular papulovesicular eruption.
  • Other less common types of id reactions include annular erythema and erythema nodosum. These patients have a strong delayed-type hypersensitivity reaction to intradermal trichophytin.
• Distribution of lesions: Skin lesions appear on the scalp with extension to the eyebrows and/or eyelashes.
• Regional lymph nodes: Cervical lymphadenopathy may develop in patients with severe inflammation associated with kerion formation.

Causes

• Infection of the scalp by dermatophytes usually is the result of person-to-person transmission. The organism remains viable on combs, brushes, couches, and sheets for long periods. Certain species of dermatophytes are endemic only in particular parts of the world. Zoophilic fungal infections of the scalp are rare.
• In the United States, T tonsurans has replaced M audouinii and M canis as the most common cause of tinea capitis. T tonsurans also is the most common cause of the disease in Canada, Mexico, and Central America.
• Historically, M audouinii was the classic causative agent in Europe and America and Microsporum ferrugineum was most common in Asia. Currently, M audouinii and M canis remain prevalent in most parts of Europe, although T violaceum also is common in Romania, Italy, Portugal, Spain, and the former USSR, as well as in Yugoslavia. In Africa, T violaceum, T schoenleinii, and M canis commonly are isolated. T violaceum and M canis are prevalent agents in Asia. T schoenleinii is common in Iran and Turkey, while M canis is common in Israel. Epidermophyton floccosum and T concentricum do not invade scalp hair. Trichophyton rubrum, which is the most common dermatophyte isolated worldwide, is not a common cause of tinea capitis.
• Dermatophytic fungi causing tinea capitis can be divided into anthropophilic and zoophilic organisms. Anthropophilic fungi grow preferentially on humans, and the most common type forms large conidia of approximately 3-4 µm in diameter within the hair shaft. Zoophilic fungi are acquired through direct contact with infected animals. Smaller conidia of approximately 1-3 µm in diameter typically are present, extending around the exterior of the hair shaft.
• Dermatophytosis customarily is divided into endothrix (inside the hair shaft) and ectothrix (extending outside the hair shaft) infection based on the location of proliferation of pathogenic fungi and destruction of the hair structure.
• Common causes of endothrix infection include T tonsurans, characterized by chains of large spores and T schoenleinii, characterized by hyphae with air spaces. Infected hairs break off sharply at the follicular orifice, leaving a conidia-filled stub or black dot. Suppuration and kerion formation (see Media File 2) commonly are associated with T tonsurans infection.
• In ectothrix infection, fragmentation of the mycelium into spores occurs just beneath the cuticle. In contrast to endothrix infection, destruction of the cuticle occurs. This type of infection is caused by T verrucosum, T mentagrophytes, and all Microsporum species.

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