INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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

Section 3 of 11  

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• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
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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.

DIFFERENTIALS

Section 4 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Other Problems to be Considered

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

Seborrheic dermatitis occurs in older children and does not cause hair loss as in tinea capitis. 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.

WORKUP

Section 5 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• Laboratory diagnosis of dermatophytosis depends on examination and culture of skin rubbings, skin or nail scrapings, hair pluckings (epilated hair), or nail clippings from lesions. 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 or toothbrush. Affected areas can be scraped 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 should be transported in a folded square of paper fastened by paper clip or scotch tape. It is easier to see affected hairs on white paper than it is 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 routine direct microscopy is 24 hours; however, culture may take several weeks. Histopathology is faster than culture for the diagnosis of onychomycosis.
  • In patients with suspected dermatophytosis of skin, any ointment or other local applications present should be removed with alcohol. Using the end of a glass slide or other implement, scale is scraped from the lesion. In cases of vesicular tinea pedis, the tops of any fresh vesicles should be removed because the fungus is often plentiful in the roof of the vesicle. In the case of tinea capitis, a moist gauze pad may be rubbed across the scalp. Broken, infected hairs adhere to the gauze. A toothbrush may be used in a similar fashion.
  • In patients suspected onychomycosis, the nail should be pared and scraped using a blunt scalpel until the crumbling, white, degenerating portion is reached. Any white keratin debris beneath the edge of the nail should be collected.
  • Skin and nail 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.
  • Up to 30% of suspicious material collected from nail specimens may be negative by either direct microscopy or culture. A positive microscopy result showing fungal hyphae and/or arthroconidia is generally sufficient for the fungus involved to be accurately identified. Repeat collections should always be considered in cases of suspected dermatophytosis that return negative laboratory reports. Histopathologic examination of clippings of a dystrophic nail and subungual debris compares favorably with other methods of diagnosis.
  • 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 on to the culture plate may yield a positive result.¹
  • 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. 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 37ºC 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 Media File 7).
  • 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.
  • In favus, infected hairs appear yellow.
• Serology is not required for a diagnosis of dermatophytosis.

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.

Fungi are seen sparsely in the stratum corneum (see Media File 5). 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 Media File 6).

In endothrix infection, spheric–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

Section 6 of 11  

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• Differentials
• Workup
• Treatment
• Medication
• Follow-up
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• References

Medical Care

Choice of treatment 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.

• Systemic administration of griseofulvin provided the first effective oral therapy for tinea capitis.
• Topical treatment alone usually is ineffective and is not recommended for the management of tinea capitis.
• Newer antifungal medications, such as ketoconazole, itraconazole, terbinafine, and fluconazole, have been reported as effective alternative therapeutic agents for tinea capitis. Of these agents, itraconazole and terbinafine are used most commonly.
• 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.

MEDICATION

Section 7 of 11  

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Griseofulvin has been the treatment of choice in all ringworm infections of the scalp. The effective dosage of griseofulvin often prescribed by specialists is 20-25 mg/kg/d for 6-8 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. Therapy 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.²

Several newer antimycotic agents, including itraconazole, terbinafine, and fluconazole, have been reported as effective and safe. Gupta et al³ 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. 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.

Terbinafine tablets at doses of 3-6 mg/kg/d for approximately 2-4 weeks have been used successfully for T tonsurans infections. M canis is relatively resistant to this drug but has been treated effectively with higher doses and longer courses of therapy. General guidelines for tinea capitis by weight include more than 40-kg body weight, 250 mg/d; 20-40 kg, 125 mg/d; and 10-20 kg, 62.5 mg/d for 2-4 weeks. This medication acts on fungal cell membranes and is fungicidal. Adverse effects include gastrointestinal disturbances and rashes in 3-5% of cases.⁴

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.

Although oral ketoconazole also is an acceptable alternative to griseofulvin, it is not considered a treatment of choice because of the risk of hepatotoxic effect and higher cost. Treatment for the deep folliculitis seen in Majocchi granuloma is systemic oral antifungal therapy.

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.

Drug Category: Antifungal agents

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.

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Further Outpatient Care

• Asymptomatic carriers who demonstrate neither signs nor symptoms of skin infection, 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.⁵
• • 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.

Deterrence/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.

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.

Prognosis

• 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.

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."

MISCELLANEOUS

Section 9 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• Failure to recognize the characteristic skin lesions on the scalp, identify the causative fungal organisms on KOH preparation (with or without a Wood fluorescent lamp), and perform biopsy examination of the affected skin (with or without fungal culture) may result in destruction of hair and pilosebaceous structures with severe hair loss and scarring alopecia. Since tinea capitis is the most common dermatophyte infection in the pediatric population in the United States, lack of accurate diagnosis and proper treatment may result in serious cosmetic impairment in young patients who are affected. The tragic detrimental effects on them are both physical and psychological. Young victims with scalp pruritus and patchy or total hair loss frequently are ridiculed and bullied by classmates or playmates. In some cases, the disease can cause emotional devastation in vulnerable uncoached children.
• Failure to identify and institute therapy in dermatophyte carriers, eg, caretakers, parents, siblings, and playmates, may hinder remedy of the disease further.

Special Concerns

• 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.⁶ 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.

MULTIMEDIA

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  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.
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Media file 2:  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.
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Media file 3:  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.
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Media file 4:  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).
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Media file 5:  Fungal hyphae and yeast cells of Trichophyton rubrum seen on the stratum corneum of tinea capitis. Periodic acid-Schiff stain, magnification 250X.
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Media file 6:  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).
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Media file 7:  Wood lamp examination of a gray-patch area on the scalp (same patient as Media File 1). In Microsporum canis infection, scalp hairs emit a diagnostic brilliant green fluorescence. Trichophyton tonsurans does not fluoresce with Wood lamp.
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REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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Article Last Updated: Jan 17, 2008