Tinea Capitis

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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.


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Gray-patch ringworm (microsporosis) is an ectothrix infection or prepubertal tinea capitis seen here in an African American male child. Gray patch ref....

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.

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.

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.[2, 3, 4, 5] 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 .[6] 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.

Mortality/Morbidity

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

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 younger than 10 years. Peak age range is in patients aged 3-7 years.

History

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.

Causes

Laboratory Studies

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.


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Photomicrograph depicting an endoectothrix invasion of a hair shaft by Microsporum audouinii. Intrapilary hyphae and spores around the hair shaft are ....

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).


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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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Pronounced inflammatory tissue reaction with follicular pustule formation surrounding a hair follicle seen in a patient with clinical form of infectio....

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.

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.

Medication Summary

Griseofulvin has been the treatment of choice in all ringworm infections of the scalp. A 2008 meta-analysis found that griseofulvin remains an effective therapy for tinea capitis.[16] Most specialists recommend a griseofulvin dosage of 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. 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.[17]

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.[18]

Gupta et al[19] 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.[20]

Terbinafine tablets at doses of 3-6 mg/kg/d for approximately 2-4 weeks have been used successfully for T tonsurans infections.[21, 22] An international study found that terbinafine has potent activity against dermatophyte isolates obtained from patients with tinea capitis worldwide.[23] 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.[24] 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.[25] M canis is relatively resistant to terbinafine but has been treated effectively with higher doses and longer courses of therapy. General guidelines for tinea capitis aretreatment for 2-4 weeks, with dosage determined by body weight, as follows:

Terbinafine acts on fungal cell membranes and is fungicidal. Adverse effects include gastrointestinal disturbances and rashes in 3-5% of cases.[26]

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.

Griseofulvin (Fulvicin)

Clinical Context:  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. Active against dermatophytes but not against yeasts or bacteria. Resistant strains of dermatophytes are rare. In its fine particle form, is absorbed readily from gut, and absorption is enhanced when fatty food is taken simultaneously. Accumulates in keratin of the stratum corneum, hair, and nails. Has a long record of safety, but newer regimens may prove more cost effective.

Itraconazole (Sporanox)

Clinical Context:  One of 2 triazole antimycotic medications with potential for treatment of superficial dermatophyte infections in pediatric population. Since it is poorly water soluble, should be taken with fatty meal to improve absorption. Most of absorbed itraconazole is bound to plasma albumin. Because of 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 wk after cessation of medication.

Hydroxyitraconazole is 1 of 30 metabolites active pharmacologically. Terminal elimination half-life of itraconazole is 20-60 h, which indicates that steady-state concentrations are reached only after at least 2 wk 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. Has significantly greater selectivity for inhibiting fungal enzymes than does ketoconazole.

Results of several clinical trials indicated that itraconazole is a safe and effective alternative to griseofulvin-failed cases. Itraconazole has slightly higher cure rate in children with tinea capitis infection caused by T violaceum, compared to treatment with terbinafine. Treatment duration is 2 wk. 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 wk, then 2 wk with no drug, followed by 1 wk with medication. When a third pulse was required, 3 wk elapsed between second and third drug treatments.

Ketoconazole (Nizoral)

Clinical Context:  Many safer alternatives are available. Usually not used to treat tinea capitis. Is a broad-spectrum synthetic antifungal compound of the azole group. When orally administered, is active against anthropophilic dermatophytes. Is hydrophilic and high concentrations of the drug develop within 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 sebum and epidermal basal layer. In the presence of normal gastric acidity, is well absorbed, and peak plasma concentrations are achieved in 3-4 d. Of the drug, 99% is bound to plasma proteins.

Extensively metabolized through oxidation and degradation of imidazole ring, O-dealkylation, oxidative degradation of 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)

Clinical Context:  Triazole compound that is relatively water soluble and well absorbed upon ingestion. Peak plasma concentration is achieved within 1-2 h after oral administration. Drug is distributed widely to body tissues, and fluids free without binding to plasma proteins. Drug has a long half-life of 22-30 h in adults, and steady-state levels are reached within 6-10 d after initiation of treatment. Most of the drug is excreted unchanged in urine with little hepatic metabolism. Eliminated slower from skin than from plasma, which contributes therapeutic benefit against superficial dermatophytosis, even after 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. Available in orange flavor oral suspension as 10-40 mg/mL.

Terbinafine (Lamisil)

Clinical Context:  Allylamine with antifungal properties. Well absorbed upon oral administration. Peak plasma concentration is reached in approximately 2 h. Drug has strong plasma protein binding. Has large lymphatic distribution and is associated with chylomicrons. Preferential uptake into fat resulted in relatively high concentration in the skin. Concentration within the stratum corneum reaches 75 times that of plasma concentration during first 2 wk of therapy. Antifungal activity remains in the skin for 2 mo after plasma concentration has depleted, following cessation of medication. Fifteen inactive metabolites following ingestion have been identified. Metabolized through N -demethylation and aromatic ring oxidation. Most metabolites are eliminated by kidneys; therefore, dosage adjustment is indicated in patients with renal or hepatic dysfunction.

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

High cure rates of fungal infections in children are reported.

Class Summary

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.

Further Outpatient Care

Deterrence/Prevention

Complications

Prognosis

Author

Grace F Kao, MD, Clinical Professor of Dermatopathology, Department of Dermatology, University of Maryland School of Medicine and George Washington University Medical School; Director, Dermatopathology Section, Department of Pathology and Laboratory Medicine, Veterans Affairs Maryland Healthcare System, Baltimore, Maryland

Disclosure: Nothing to disclose.

Specialty Editors

Franklin Flowers, MD, Chief, Division of Dermatology, Professor, Department of Medicine and Otolaryngology, Affiliate Associate Professor of Pediatrics and Pathology, University of Florida College of Medicine

Disclosure: Nothing to disclose.

Michael J Wells, MD, Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

Disclosure: Nothing to disclose.

Paul Krusinski, MD, Director of Dermatology, Fletcher Allen Health Care; Professor, Department of Internal Medicine, University of Vermont College of Medicine

Disclosure: Nothing to disclose.

Joel M Gelfand, MD, MSCE, Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania

Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds Investigator; Genentech Grant/research funds investigator; Centocor Consulting fee Consulting; Abbott Grant/research funds investigator; Abbott Consulting fee Consulting; Novartis investigator; Pfizer Grant/research funds investigator; Celgene Consulting fee DMC Chair; NIAMS and NHLBI Grant/research funds investigator

Chief Editor

Dirk M Elston, MD, Director, Ackerman Academy of Dermatopathology, New York

Disclosure: Nothing to disclose.

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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.

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.

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.

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.

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.

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.

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.

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).

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 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).

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.

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.

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.

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).

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 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).

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.