Tinea Capitis 

Updated: Jun 13, 2018
Author: Marc Zachary Handler, MD; Chief Editor: Dirk M Elston, MD 

Overview

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 (see the image below). 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.[1]

Gray-patch ringworm (microsporosis) is an ectothri Gray-patch ringworm (microsporosis) is an ectothrix infection or prepubertal tinea capitis seen here in an African American male child. Gray patch refers to the scaling with lack of inflammation, as noted in this patient. Hairs in the involved areas assume a characteristic dull, grayish, discolored appearance. Infected hairs are broken and shorter. Papular lesions around hair shafts spread and form typical patches of ring forms, as shown. Culture from the lesional hair grew Microsporum canis.

See 15 Rashes You Need to Know: Common Dermatologic Diagnoses, a Critical Images slideshow, for help identifying and treating various rashes.

Also, see the 15 Back-to-School Illnesses You Should Know slideshow to help identify conditions that may occur in young patients after they return to the classroom.

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 are among the most common infectious agents of humans, causing a variety of clinical conditions that are collectively 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.

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.[2]

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).[3]

Favus, usually caused by T schoenleinii, produces favuslike crusts or scutula and corresponding hair loss.

Etiology

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 M 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.[4] T violaceum and M canis are prevalent agents in Asia.[5] 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 the image below) commonly are associated with T tonsurans infection.

Typical lesions of kerion celsi on the vertex scal Typical lesions of kerion celsi on the vertex scalp of a young Chinese boy. Note numerous bright yellow purulent areas on skin surface, surrounded by adjacent edematous, erythematous, alopecic areas. Culture from the lesion grew Trichophyton mentagrophytes. Courtesy of Skin Diseases in Chinese by Yau-Chin Lu, MD. Permission granted by Medicine Today Publishing Co, Taipei, Taiwan, 1981.

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.

Epidemiology

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, at rates of 12.9%.[6] In Northern California, the reported incidence among the pediatric population is 0.34%.[7]

Tinea capitis is predominantly a disease of preadolescent children. Typical age of onset is between 5 and 10 years.[6] Tinea capitis 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.[8, 9, 10, 11] In Ethiopia, the incidence of tinea capitis is 8.7% among children aged 4-14 years.[12] 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 .[13] 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) occurs in rural areas.

Sex

The incidence of tinea capitis may vary by sex, depending on the causative fungal organism. Microsporum audouinii –related tinea capitis has been reported to be up to 5 times more common in boys than in girls. After puberty, however, the reverse is true, possibly because of women having greater exposure to infected children and possibly because of hormonal factors. In infection by M canis, the ratio varies, but the infection rate usually is higher in boys. 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 aged between 5 and 10 years.[6] Mean age of onset is in patients aged 6.9-8.1 years.[7]

Prognosis

Tinea capitis carries a positive prognosis, with the vast majority of those treated obtaining resolution of the infection. Those who have maintained untreated or resistant-to-treatment tinea capitis are at risk for abscess development, referred to as a kerion.[14]  

Continuous shedding of fungal spores may last several months despite active treatment; therefore, keeping patients with tinea capitis out of school is impractical. The causes of treatment failure include reinfection, relative insensitivity of the organism, suboptimal absorption of the medication, and lack of compliance with the long courses of treatment. T tonsurans and Microsporum species are typical offending agents in persistent positive cases. If fungi can still be isolated from the lesional skin at the completion of treatment, but clinical signs have improved, the recommendation is to continue the original regimen for another month.

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 the image below). Some ectothrix infections involute during the normal course of disease without treatment. Depending on the extent of associated inflammation, lesions may heal with scarring.

Gray-patch ringworm (microsporosis) is an ectothri Gray-patch ringworm (microsporosis) is an ectothrix infection or prepubertal tinea capitis seen here in an African American male child. Gray patch refers to the scaling with lack of inflammation, as noted in this patient. Hairs in the involved areas assume a characteristic dull, grayish, discolored appearance. Infected hairs are broken and shorter. Papular lesions around hair shafts spread and form typical patches of ring forms, as shown. Culture from the lesional hair grew Microsporum canis.

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.

Patient Education

Patient education is paramount in eradicating tinea capitis. The current recommendations of the Committee on Infectious Diseases of the American Academy of Pediatrics state that "Children receiving treatment for tinea capitis may attend school. Haircuts, shaving of the head, wearing a cap during treatment are not necessary."

 

Presentation

History

Tinea capitis 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. Ring-shaped 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 the image below).

Typical lesions of kerion celsi on the vertex scal Typical lesions of kerion celsi on the vertex scalp of a young Chinese boy. Note numerous bright yellow purulent areas on skin surface, surrounded by adjacent edematous, erythematous, alopecic areas. Culture from the lesion grew Trichophyton mentagrophytes. Courtesy of Skin Diseases in Chinese by Yau-Chin Lu, MD. Permission granted by Medicine Today Publishing Co, Taipei, Taiwan, 1981.

Favus (also termed tinea favosa) is a severe form of tinea capitis. Favus is a chronic infection 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 Examination

A variety of clinical presentations of tinea capitis are recognized as being inflammatory or noninflammatory and are usually associated with patchy alopecia. Physical examination with a hand lens or trichoscopy may be helpful in demonstrating the affected hairs.[15, 16, 17] The infection may be widespread, and the clinical appearances can be subtle, especially in black children with Trichophyton tonsurans infection, in whom the findings may mimic patches of seborrheic dermatitis with hair loss. 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.

T tonsurans is the most common pathogen causing tinea capitis in the United States. As T tonsurans is an endothrix, its spores remain inside the hair shaft and do not fluoresce at Wood lamp examination. Thus, diagnosis should be made with mycological analysis by scraping scale from the scalp and sending it to the laboratory for confirmation of diagnosis. As M canis and M audouinii do exist in the United States, as with other species that cause tinea capitis, it is suggested to perform a Wood lamp examination, evaluating for an ectothrix infection of the hairs. If positive, the hairs fluoresce.[14]

Pertinent physical findings are limited to the skin of scalp, eyebrows, and eyelashes.[18]

Primary skin lesions of tinea capitis

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 the image below). This is often described as having a “moth-eaten" appearance.

Discrete patches of hair loss or alopecia caused b Discrete patches of hair loss or alopecia caused by Trichophyton violaceum infection of the vertex scalp of a young Taiwanese boy. Courtesy of Skin Diseases in Chinese by Yau-Chin Lu, MD. Permission granted by Medicine Today Publishing Co, Taipei, Taiwan, 1981.

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 tinea capitis 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.

Complications

The causative fungal organisms of tinea capitis destroy hair and pilosebaceous structures, resulting in severe hair loss and scarring alopecia. Since tinea capitis is the most common dermatophyte infection in the pediatric population in the United States, without accurate diagnosis and proper treatment, the disease is detrimental, both physically and mentally, to children who are affected. Young patients with itchy scalp and patchy or total hair loss frequently are ridiculed, isolated, and bullied by classmates or playmates. In some cases, the disease can cause severe emotional impairment in vulnerable children and can destabilize family relationships.

 

DDx

Diagnostic Considerations

Also consider the following:

  • Bacterial folliculitis
  • Dissecting folliculitis (folliculitis decalvans)
  • Abscess
  • Neoplasia
  • Pyoderma
  • Secondary syphilis

Seborrheic dermatitis occurs in older children and, unlike tinea capitis, does not cause hair loss. In some cases of tinea capitis, the erythematous scaly lesions closely resemble those seen in seborrheic dermatitis; however, in seborrheic dermatitis, hairs are not broken. Seborrheic dermatitis and psoriasis may cause accumulation of scales in matted masses on the scalp. Scales are more prominent in psoriasis, and hairs are not broken.

Impetigo may be difficult to distinguish from inflammatory tinea capitis, although pain is less severe in tinea capitis, and hairs tend to be seated firmly in impetigo. Alopecia areata also causes circumscribed areas of hair loss similar to tinea capitis, but alopecia areata does not cause scaling. Lesions may have an erythematous border in the early stages of the disease, but this reverses to normal color at later stages. The exclamation mark hairs seen in alopecia areata, in which broken hairs taper from the fractured end toward the skin surface, are pathognomonic.

In secondary syphilis, areas of alopecia have a characteristic moth-eaten appearance or resemble alopecia areata. Serologic testing for the presence of treponemal antibody (rapid plasma reagin and Treponema -specific tests, eg, microhemagglutination– Treponema pallidum test) and testing by special silver impregnation histochemical stain (Warthin-Starry stain) for the demonstration of treponemal organisms aid in the accurate diagnosis of syphilis.

The patient may present with a generalized eruption of itchy papules, particularly around the outer helix of the ear, occurring as a reactive phenomenon (an id response). These symptoms may start with the introduction of systemic treatment for tinea capitis; thus, they be mistaken for a drug reaction.

Differential Diagnoses

 

Workup

Laboratory Studies

Culture

Laboratory diagnosis of tinea capitis depends on examination and culture of skin rubbings, skin scrapings, or hair pluckings (epilated hair) from lesions.

Before specimen collection, any ointment or other local applications present should be removed with alcohol.

Infected hairs appearing as broken stubs are best for examination. They can be removed with forceps without undue trauma or collected by gentle rubbing with a moist gauze pad; broken, infected hairs adhere to the gauze. A toothbrush may be used in a similar fashion.[19] Alternatively, affected areas can be scraped with the end of a glass slide or with a blunt scalpel to harvest affected hairs, broken-off hair stubs, and scalp scale. This is preferable to plucking, which may remove uninvolved hairs. Scrapings may be transported in a folded square of paper. Skin specimens may be scraped directly onto special black cards, which make it easier to see how much material has been collected and provide ideal conditions for transportation to the laboratory; however, affected hairs are easier to see on white paper than on black paper.

Definitive diagnosis depends on an adequate amount of clinical material submitted for examination by direct microscopy and culture. The turn-around time for culture may take several weeks.

Selected hair samples are cultured or allowed to soften in 10-20% potassium hydroxide (KOH) before examination under the microscope. Examination of KOH preparations (KOH mount) usually determines the proper diagnosis if a tinea infection exists.

Conventional sampling of a kerion can be difficult. Negative results are not uncommon in these cases. The diagnosis and decision to treat lesions of kerion may need to be made clinically. A moistened standard bacteriological swab taken from the pustular areas and inoculated onto the culture plate may yield a positive result.[20]

Microscopic examination of the infected hairs may provide immediate confirmation of the diagnosis of ringworm and establishes whether the fungus is small-spore or large-spore ectothrix or endothrix.

Culture provides precise identification of the species for epidemiologic purposes.[21] Primary isolation is carried out at room temperature, usually on Sabouraud agar containing antibiotics (penicillin/streptomycin or chloramphenicol) and cycloheximide (Acti-Dione), which is an antifungal agent that suppresses the growth of environmental contaminant fungi. In cases of tender kerion, the agar plate can be inoculated directly by pressing it gently against the lesion. Most dermatophytes can be identified within 2 weeks, although T verrucosum grows best at 37°C and may have formed only into small and granular colonies at this stage. Identification depends on gross colony and microscopic morphology. Specimens should be inoculated on to primary isolation media, such as Sabouraud dextrose, and incubated at 26-28°C for 4 weeks. The growth of any dermatophyte is significant.

In some cases, other tests involving nutritional requirements and hair penetration in vitro are necessary to confirm the identification.

Wood lamp examination

In 1925, Margarot and Deveze observed that infected hairs and some fungus cultures fluoresce in ultraviolet light. The black light commonly is termed Wood lamp. Light is filtered through a Wood nickel oxide glass (barium silicate with nickel oxide), which allows only the long ultraviolet rays to pass (peak at 365 nm). Wood lamp examination is useful for certain ectothrix infections (eg, those caused by M canis,M audouinii,Microsporum rivalieri). In cases with endothrix infection, however, negative Wood lamp examination findings are of no practical value for screening or monitoring infections.

Hairs infected by M canis, M audouinii, M rivalieri, and M ferrugineum fluoresce a bright green to yellow-green color (see the image below).

Wood lamp examination of a gray-patch area on the Wood lamp examination of a gray-patch area on the scalp. In Microsporum canis infection, scalp hairs emit a diagnostic brilliant green fluorescence. Trichophyton tonsurans does not fluoresce with Wood lamp.

Hairs infected by T schoenleinii may show a dull green or blue-white color, and hyphae regress leaving spaces within the hair shaft. T verrucosum exhibits a green fluorescence in cow hairs, but infected human hairs do not fluoresce. The fluorescent substance appears to be produced by the fungus only in actively growing infected hairs. Infected hairs remain fluorescent for many years after the arthroconidia have died.

When a diagnosis of ringworm is under consideration, the scalp is examined under a Wood lamp. If fluorescent infected hairs are present, hairs are removed for light microscopic examination and culture. Infections caused by Microsporum species fluoresce a typical green color.

Unfortunately, most tinea capitis infections in North America are caused by T tonsurans and do not demonstrate fluorescence.[22]

In favus, infected hairs appear yellow (see the image below).

Wood lamp examination of a gray-patch area on the Wood lamp examination of a gray-patch area on the scalp. In Microsporum canis infection, scalp hairs emit a diagnostic brilliant green fluorescence. Trichophyton tonsurans does not fluoresce with Wood lamp.

Serology

Serology  is not required for a diagnosis of dermatophytosis.

Videodermatoscopy

A small study in patients with tinea capitis from M canis found that comma hairs were a prominent and distinctive feature on videodermatoscopy; comma hairs were not seen in patients with alopecia areata.[23]

Histologic Findings

Skin biopsy with particular emphasis on examination of infected hairs with special histochemical stains aids in the identification of the causative fungus, especially in cases of fungal folliculitis (Majocchi granuloma) and onychomycosis. Bullous tinea demonstrates subepidermal edema and reticular degeneration of the epidermis. Tinea corporis demonstrates subacute and chronic dermatitis with or without follicular inflammation and destruction. Suppurative folliculitis may be present. In the mildest form, hyperkeratosis, parakeratosis, spongiosis, slight vasodilatation, and a perivascular inflammatory infiltrate in the upper dermis are present. Fungal hyphae can be demonstrated using routine hematoxylin and eosin stain, and identification can be facilitated by using special stains. Periodic acid-Schiff stain with diastase digestion or counterstained with green dye facilitates identification of fungal elements. See the image below.

Photomicrograph depicting an endoectothrix invasio Photomicrograph depicting an endoectothrix invasion of a hair shaft by Microsporum audouinii. Intrapilary hyphae and spores around the hair shaft are seen (hematoxylin and eosin stain with Periodic acid-Schiff counterstain, magnification X 250).

Fungi are seen sparsely in the stratum corneum (see the first image below). Hyphae extend down the hair follicle, growing on the surface of the hair shaft. Hyphae then invade the hair, penetrate the outermost layer of hair (ie, cuticle), and proliferate downward in the subcuticular portion of the cortex, gradually penetrating deep into the hair cortex. Pronounced inflammatory tissue reaction with follicular pustule formation surrounding hair follicles is seen in patients with the clinical form of infection termed kerion celsi (see the second image below).

Fungal hyphae and yeast cells of Trichophyton rubr Fungal hyphae and yeast cells of Trichophyton rubrum seen on the stratum corneum of tinea capitis. Periodic acid-Schiff stain, magnification 250X.
Pronounced inflammatory tissue reaction with folli Pronounced inflammatory tissue reaction with follicular pustule formation surrounding a hair follicle seen in a patient with clinical form of infection, termed kerion celsi. No fungal hyphae or spores were identified in the lesion in either tissue sections or culture. Fluorescein-labeled Trichophyton mentagrophytes antiserum cross-reacted with antigens of dermatophyte in the infected hairs within the pustule (hematoxylin and eosin stain, magnification X 75).

In endothrix infection, spherical–to–box-like spores are found within the hair shaft. This type of infection is caused by T tonsurans or T violaceum.

In ectothrix infection, organisms form a sheath around the hair shaft. In contrast to endothrix infection, destruction of the cuticle by hyphae and spores occurs.

 

Treatment

Medical Care

Choice of treatment for tinea capitis is determined by the species of fungus concerned, the degree of inflammation, and in some cases, by the immunologic and nutritional status of the patient.

After microscopic or culture confirmation, medical therapy should be initiated. Systemic administration of griseofulvin provided the first effective oral therapy for tinea capitis, and resistance to the medication has remained minimal.[24, 25, 26] Dosing in the pediatric population is weight based. Recommended dosing is 20-25 mg/kg/day in single or two divided doses for microsized griseofulvin or 15-20 mg/kg/day in single dose or two divided doses for ultramicrosized griseofulvin.[27] The duration of treatment should be between 4 and 6 weeks.

Topical treatment alone usually is ineffective and is not recommended for the management of tinea capitis.

Newer antifungal medications, such as itraconazole, terbinafine, and fluconazole, have been reported as effective alternative therapeutic agents for tinea capitis.[24, 25]  Of these agents, itraconazole and terbinafine are used most commonly. There may be some advantage to giving itraconazole with whole milk to increase absorption.[28]  Data suggest that itraconazole and terbinafine have the highest mycological cure rates in children (79% and 81%, respectively), while griseofulvin and terbinafine have the highest complete cure rate (72% and 92%, respectively). Griseofulvin is more effective against Microsporum infections, while terbinafine and itraconazole are more effective in Trichophyton infections.[29] It should be noted that responses may vary geographically.[30]

Selenium sulfide shampoo may reduce the risk of spreading the infection early in the course of therapy by reducing the number of viable spores that are shed.

Prevention

Asymptomatic carriers should be detected and treated, since they are the continuous source of infection. Siblings and playmates of patients should avoid close physical contact and sharing of toys or other personal objects, such as combs and hairbrushes, since organisms can spread from one person to another and infectious agents can be transported to different classrooms within the same or in different schools. Shared facilities and objects also may promote spread of disease, both within the home and the classroom.

Public health measures regarding the source of infection should be a concern for controlling tinea capitis.

The source of some zoophilic species often is difficult to trace. Outbreaks of M canis can be extensive. Patients' cats and dogs must be inspected under a Wood lamp and referred for treatment. At times, animal control agencies are contacted to round up stray dogs and cats. T mentagrophytes may follow known contact with rodents, but often, no source can be identified.

As many as 14% of asymptomatic children have been found to be carriers of causative dermatophyte for tinea capitis in a primary school in Philadelphia.[31] Without therapy, 4% developed symptoms of infection, 58% remained culture positive, and 38% became culture negative within an average 2.3-month follow-up period.

Long-Term Monitoring

Household contacts of tinea capitis patients should be screened for clinically silent fungal carriage on the scalp.[32] Asymptomatic carriers, including adults and siblings in the family of patients with tinea capitis and patient caretakers and playmates, require active treatment, since they may act as a continuing source of infection.[33]

Shampoo and oral antimycotic therapy have been advocated for eradication of the carrier state. Studies have shown that most children who received griseofulvin plus biweekly shampooing with 2.5% selenium sulfide were negative for fungi on scalp culture after 2 weeks. Shampoo containing povidone-iodine has been shown to be more effective in producing negative cultures than shampoos containing econazole and selenium sulfide and than Johnson's Baby Shampoo. Therapeutic shampoos are applied twice weekly for 15 minutes for 4 consecutive weeks. Both povidone-iodine and selenium shampoos require further clinical study for the control of fungal spore loads in infected children and asymptomatic carriers.

Classrooms with young children (ie, kindergarten through second grade) must be evaluated for tinea capitis infection, since these children are most susceptible and have a greater risk of disease transmission.

Playmates in close physical contact with patients can spread tinea capitis organisms by sharing toys or personal objects including combs and hairbrushes. These individuals need to be evaluated for the presence of infection.

 

Medication

Medication Summary

Griseofulvin has been the traditional treatment of choice in all ringworm infections of the scalp. A 2008 meta-analysis found that griseofulvin remains an effective therapy for tinea capitis.[34] Most specialists recommend a griseofulvin dosage of 20-25 mg/kg/d for 4-6 weeks. Griseofulvin accumulates in keratin of the horny layer, hair, and nails, rendering them resistant to invasion by the fungus. Treatment must continue long enough for infected keratin to be replaced by resistant keratin, usually 4-6 weeks. In inflammatory lesions, compresses often are required to remove pus and infected scale. Therapeutic progress is monitored by regular clinical examination with the aid of a Wood lamp for fluorescent species such as M audouinii and M canis. Adverse effects include nausea and rashes in 8-15%. The drug is contraindicated in pregnancy, and the manufacturers caution against men fathering a child for 6 months following treatment.[35]

Several newer antimycotic agents, including itraconazole, terbinafine, and fluconazole, have been reported as effective and safe. A review found that these agents may be similar to griseofulvin for treatment in children with tinea capitis caused by Trichophyton species and have the advantage of shorter treatment durations; however, they may be more expensive.[36]

Gupta et al[37] reported the following alternative effective and safe treatment regimens for tinea capitis with endothrix species infection including T tonsurans: itraconazole continuous regimen (3-5 mg/kg/d with a full meal for 4-6 wk), itraconazole pulse regimen with capsules (5 mg/kg/d for 1 wk times 3 pulses 3 wk apart), and itraconazole pulse regimen with oral solution (3 mg/kg/d for 1 wk times 3 pulses, ie, 1 wk per mo). The oral solution contains cyclodextrin, which may cause diarrhea in children. The pharmacokinetics of the liquid formulation are not well established in children. In some children (weighing 20-40 kg), a single 100-mg capsule daily for 4-6 weeks has been used successfully.

Because itraconazole has been associated with heart failure, it is currently not favored as a first-line therapy for tinea. An exception may be serious M canis infections, which are relatively insensitive to terbinafine, or, according to some authors, if griseofulvin is not available.[38]

Terbinafine tablets at doses of 3-6 mg/kg/d for approximately 2-4 weeks have been used successfully for T tonsurans infections.[39, 40] An international study found that terbinafine has potent activity against dermatophyte isolates obtained from patients with tinea capitis worldwide.[41] A pediatric study found terbinafine produced significantly better cure rates than griseofulvin for tinea capitis caused by T tonsurans but not for disease caused by M canis.[42] A meta-analysis of 7 studies concluded that terbinafine was more effective for tinea capitis primarily caused by Trichophyton species, whereas griseofulvin was more effective for tinea capitis primarily caused by Microsporum species.[43] M canis is relatively resistant to terbinafine but has been treated effectively with higher doses and longer courses of therapy. 

Terbinafine acts on fungal cell membranes and is fungicidal. Adverse effects include gastrointestinal disturbances and rashes in 3-5% of cases.[44]

Fluconazole tablets or oral suspension (3-6 mg/kg/d) are administered for 6 weeks. In 1 trial, a dose of 6 mg/kg/d for 20 days was effective. An extra week of therapy (6 mg/kg/d) can be administered if clinically indicated at that time.

In ectothrix infection (eg, M audouinii, M canis), a longer duration of therapy may be required.

Oral ketoconazole is rarely an acceptable alternative to griseofulvin because of the risk of hepatotoxic effect and higher cost.[45]

Oral steroids may help reduce the risk for and extent of permanent alopecia in the treatment of kerion. Avoid using topical corticosteroids during treatment of dermatophyte infections.

Antifungal agents

Class Summary

The mechanism of action may involve an alteration of RNA and DNA metabolism or an intracellular accumulation of peroxide that is toxic to the fungal cell.

Griseofulvin (Fulvicin)

Griseofulvin is an antibiotic derived from a Penicillium species that is deposited in the keratin precursor cells that are replaced gradually by noninfected tissue. As a result, new keratin becomes highly resistant to fungal invasions. It is active against dermatophytes but not against yeasts or bacteria. Resistant strains of dermatophytes are rare. In its fine particle form, it is absorbed readily from the gut, and absorption is enhanced when fatty food is taken simultaneously. Griseofulvin accumulates in the keratin of the stratum corneum, hair, and nails. It has a long record of safety, but newer regimens may prove more cost effective.

Itraconazole (Sporanox)

Itraconazole is one of two triazole antimycotic medications with the potential for treatment of superficial dermatophyte infections in the pediatric population. Since it is poorly water soluble, it should be taken with a fatty meal to improve absorption. Most of the  absorbed itraconazole is bound to plasma albumin. Because of its lipophilic property, it is found in highest concentrations in fat, omentum, skin, nails, and vaginal and cervical tissues. Antimycotically significant concentrations may remain in skin up to 4 weeks after cessation of medication.

Hydroxyitraconazole is one of 30 metabolites active pharmacologically. The terminal elimination half-life of itraconazole is 20-60 hours, which indicates that steady-state concentrations are reached only after at least 2 weeks of daily administration. Large biliary excretion of itraconazole and its metabolites occurs because of their large molecular sizes and high molecular weights. They are excreted 65% in feces and 35% in urine. No indication exists for dosage adjustment for impaired hepatic and renal functions. Itraconazole has significantly greater selectivity for inhibiting fungal enzymes than does ketoconazole.

The results of several clinical trials indicated that itraconazole is a safe and effective alternative to griseofulvin-failed cases. Itraconazole has a slightly higher cure rate in children with tinea capitis infection caused by T violaceum, compared with treatment with terbinafine. The treatment duration is 2 weeks. In children with T tonsurans infection treated with 1-3 pulses of itraconazole, a 100% cure rate has been reported by Gupta et al in a small series. The pulse schedule was itraconazole 5 mg/kg/d for 1 week, then 2 weeks with no drug, followed by 1 week with medication. When a third pulse was required, 3 weeks elapsed between the second and third drug treatments.

Ketoconazole (Nizoral)

Many safer alternatives are available. Ketoconazole is rarely used to treat tinea capitis. It is a broad-spectrum synthetic antifungal compound of the azole group. When orally administered, it is active against anthropophilic dermatophytes. It is hydrophilic and high concentrations of the drug develop within the skin, making it potentially beneficial for treating superficial dermatophytosis. Delivery of this drug to the skin is accomplished through normal blood circulation and sweat. Some excretion occurs into the sebum and epidermal basal layer. In the presence of normal gastric acidity, it is well absorbed, and peak plasma concentrations are achieved in 3-4 days. Of the drug, 99% is bound to plasma proteins.

Ketoconazole is extensively metabolized through oxidation and degradation of the imidazole ring, O-dealkylation, oxidative degradation of the piperazine ring, and aromatic hydroxylation. Untransformed ketoconazole is the only active antifungal compound. None of the metabolites possesses therapeutic activity.

Despite active metabolism, ketoconazole is excreted in bile and eliminated unchanged. Dosage adjustment is not required in patients with impaired renal function in view of the rapid metabolism and active biliary excretion.

Fluconazole (Diflucan)

Fluconazole is a triazole compound that is relatively water soluble and well absorbed upon ingestion. Peak plasma concentration is achieved within 1-2 hours after oral administration. The drug is distributed widely to body tissues, and fluids free without binding to plasma proteins. The drug has a long half-life of 22-30 hours in adults, and steady-state levels are reached within 6-10 days after initiation of treatment. Most of the drug is excreted unchanged in urine with little hepatic metabolism. It is eliminated slower from skin than from plasma, which contributes therapeutic benefits against superficial dermatophytosis, even after the dosage has been discontinued. Dosage adjustment is required for patients with renal impairment, since drug is eliminated primarily by the kidneys.

More dosing regimen studies are needed. It is available in orange flavor oral suspension as 10-40 mg/mL.

Terbinafine (Lamisil)

Terbinafine is an allylamine with antifungal properties. It is well absorbed upon oral administration. The peak plasma concentration is reached in approximately 2 hours. The drug has strong plasma protein binding. It has a large lymphatic distribution and is associated with chylomicrons. Preferential uptake into fat results in relatively high concentrations in the skin. Concentration within the stratum corneum reaches 75 times that of plasma concentration during first 2 weeks of therapy. Antifungal activity remains in the skin for 2 months after the plasma concentration has depleted, following cessation of medication. Fifteen inactive metabolites following ingestion have been identified. Terbinafine is metabolized through N -demethylation and aromatic ring oxidation. Most metabolites are eliminated by the kidneys; therefore, a dosage adjustment is indicated in patients with renal or hepatic dysfunction.

Compared with itraconazole, terbinafine has a slightly lower cure rate; 4 weeks of treatment with terbinafine is reported as effective as 8 weeks of griseofulvin therapy.

High cure rates of fungal infections in children are reported.

 

Questions & Answers

Overview

What is tinea capitis (ringworm of the scalp)?

What are the types of dermatophytosis?

How does the clinical presentation of tinea capitis vary?

When were the causes and treatment of tinea capitis (scalp ringworm) first identified?

What is the pathophysiology of tinea capitis (scalp ringworm)?

What causes tinea capitis (scalp ringworm)?

What is the role of dermatophytes in the pathophysiology of tinea capitis (scalp ringworm)?

How is in vivo hair invasion characterized in the pathophysiology of tinea capitis (scalp ringworm)?

How are dermatophytes transmitted in tinea capitis (scalp ringworm)?

How does the causative agent of tinea capitis (scalp ringworm) vary by geographic location?

How are the dermatophytic fungi that cause tinea capitis (scalp ringworm) classified?

How is dermatophytosis characterized?

What are the common causes of tinea capitis (scalp ringworm)?

What is the incidence of tinea capitis (scalp ringworm) in the US?

What is the global incidence of tinea capitis (scalp ringworm)?

How does the incidence of tinea capitis (scalp ringworm) vary by sex?

How does the incidence of tinea capitis (scalp ringworm) vary by age?

What is the prognosis of tinea capitis (scalp ringworm)?

How is the classification and severity of tinea capitis (scalp ringworm) determined?

How is ectothrix infection in tinea capitis (scalp ringworm) defined?

What is the prognosis of endothrix infections in tinea capitis (scalp ringworm)?

What are the AAP recommendations for children during tinea capitis (scalp ringworm) treatment?

Presentation

What is the disease course of tinea capitis (scalp ringworm)?

Which presentations are characteristic of tinea capitis (scalp ringworm)?

What is favus?

Which physical findings suggest tinea capitis (scalp ringworm)?

How is tinea capitis (scalp ringworm) diagnosed?

What should be included in the physical exam of tinea capitis (scalp ringworm)?

Which physical findings of skin lesions suggest tinea capitis (scalp ringworm)?

What are the physical findings of dermatophyte id reactions in tinea capitis (scalp ringworm)?

What is the distribution of tinea capitis (scalp ringworm) lesions?

What increases the risk of cervical lymphadenopathy in tinea capitis (scalp ringworm)?

What are possible complications of tinea capitis (scalp ringworm)?

DDX

Which conditions should be included in the differential diagnoses of tinea capitis (scalp ringworm)?

How is seborrheic dermatitis differentiated from tinea capitis (scalp ringworm)?

How is impetigo differentiated from tinea capitis (scalp ringworm)?

How is secondary syphilis differentiated from tinea capitis (scalp ringworm)?

What are the differential diagnoses for Tinea Capitis?

Workup

What is the role of serology in the diagnosis of tinea capitis (scalp ringworm)?

How is tinea capitis (scalp ringworm) diagnosed?

What is the proper procedure prior to specimen collection for the diagnosis of tinea capitis (scalp ringworm)?

How are infected hairs collected for diagnosis of tinea capitis (scalp ringworm)?

What is needed to definitively diagnosis tinea capitis (scalp ringworm)?

How are hair samples handled before evaluation for tinea capitis (scalp ringworm)?

What is the role of kerion sampling in the diagnosis of tinea capitis (scalp ringworm)?

What can be determined by microscopic exam of infected hairs in tinea capitis (scalp ringworm)?

What is the role of cultures in the diagnosis of tinea capitis (scalp ringworm)?

What is the role of Wood lamp exam in the diagnosis of tinea capitis (scalp ringworm)?

When is Wood lamp exam indicated in the workup of tinea capitis (scalp ringworm)?

What findings on videodermatoscopy suggest tinea capitis (scalp ringworm)?

What is the role of skin biopsy in the diagnosis of tinea capitis (scalp ringworm)?

Which histologic findings are characteristic of tinea capitis (scalp ringworm)?

Treatment

What is the basis for treatment selection for tinea capitis (scalp ringworm)?

What is the role of griseofulvin in the treatment of tinea capitis?

Which medications are effective for treatment of tinea capitis (scalp ringworm)?

How can tinea capitis (scalp ringworm) be prevented?

Why should asymptomatic tinea capitis (scalp ringworm) be treated?

What is the efficacy of shampoo and oral antimycotic therapy for the treatment of tinea capitis (scalp ringworm)?

Who must be evaluated for tinea capitis (scalp ringworm)?

How may tinea capitis (scalp ringworm) spread among children?

Medications

What is the treatment of choice for tinea capitis (scalp ringworm)?

What agents are effective and safe for treatment of tinea capitis (scalp ringworm)?

What is the role of itraconazole in the treatment of tinea capitis (scalp ringworm)?

What is the role of terbinafine for the treatment of tinea capitis (scalp ringworm)?

What is the role of fluconazole for the treatment of tinea capitis (scalp ringworm)?

What may be required for treatment of ectothrix infections of tinea capitis (scalp ringworm)?

What is the role of ketoconazole for the treatment of tinea capitis (scalp ringworm)?

How are steroids used in the treatment of tinea capitis (scalp ringworm)?

Which medications in the drug class Antifungal agents are used in the treatment of Tinea Capitis?