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.
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.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.
- 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.
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. 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) occurs 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 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 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.
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.
Seebacher C, Bouchara JP, Mignon B. Updates on the epidemiology of dermatophyte infections. Mycopathologia. Nov-Dec 2008;166(5-6):335-52. [Medline].
Kondo M, Nakano N, Shiraki Y, Hiruma M, Ikeda S, Sugita T. A Chinese-Japanese boy with black dot ringworm due to Trichophyton violaceum. J Dermatol. Mar 2006;33(3):165-8. [Medline].
Akbaba M, Ilkit M, Sutoluk Z, Ates A, Zorba H. Comparison of hairbrush, toothbrush and cotton swab methods for diagnosing asymptomatic dermatophyte scalp carriage. J Eur Acad Dermatol Venereol. Mar 2008;22(3):356-62. [Medline].
Friedlander SF, Pickering B, Cunningham BB, Gibbs NF, Eichenfield LF. Use of the cotton swab method in diagnosing Tinea capitis. Pediatrics. Aug 1999;104(2 Pt 1):276-9. [Medline].
Bonifaz A, Isa-Isa R, Araiza J, Cruz C, Hernández MA, Ponce RM. Cytobrush-culture method to diagnose tinea capitis. Mycopathologia. Jun 2007;163(6):309-13. [Medline].
Trovato MJ, Schwartz RA, Janniger CK. Tinea capitis: current concepts in clinical practice. Cutis. Feb 2006;77(2):93-9. [Medline].
Slowinska M, Rudnicka L, Schwartz RA, et al. Comma hairs: a dermatoscopic marker for tinea capitis: a rapid diagnostic method. J Am Acad Dermatol. Nov 2008;59(5 Suppl):S77-9. [Medline].
Gupta AK, Cooper EA, Bowen JE. Meta-analysis: griseofulvin efficacy in the treatment of tinea capitis. J Drugs Dermatol. Apr 2008;7(4):369-72. [Medline].
Fleece D, Gaughan JP, Aronoff SC. Griseofulvin versus terbinafine in the treatment of tinea capitis: a meta-analysis of randomized, clinical trials. Pediatrics. Nov 2004;114(5):1312-5. [Medline].
[Best Evidence] Gonzalez U, Seaton T, Bergus G, Jacobson J, Martinez-Monzon C. Systemic antifungal therapy for tinea capitis in children. Cochrane Database Syst Rev. Oct 17 2007;CD004685. [Medline].
Gupta AK, Hofstader SL, Adam P, Summerbell RC. Tinea capitis: an overview with emphasis on management. Pediatr Dermatol. May-Jun 1999;16(3):171-89. [Medline].
Koumantaki-Mathioudaki E, Devliotou-Panagiotidou D, Rallis E, et al. Is itraconazole the treatment of choice in Microsporum canis tinea capitis?. Drugs Exp Clin Res. 2005;31 Suppl:11-5. [Medline].
Friedlander SF, Aly R, Krafchik B, et al. Terbinafine in the treatment of Trichophyton tinea capitis: a randomized, double-blind, parallel-group, duration-finding study. Pediatrics. Apr 2002;109(4):602-7. [Medline].
Krafchik B, Pelletier J. An open study of tinea capitis in 50 children treated with a 2-week course of oral terbinafine. J Am Acad Dermatol. Jul 1999;41(1):60-3. [Medline].
Ghannoum MA, Wraith LA, Cai B, Nyirady J, Isham N. Susceptibility of dermatophyte isolates obtained from a large worldwide terbinafine tinea capitis clinical trial. Br J Dermatol. Sep 2008;159(3):711-3. [Medline].
[Best Evidence] Elewski BE, Caceres HW, DeLeon L, et al. Terbinafine hydrochloride oral granules versus oral griseofulvin suspension in children with tinea capitis: results of two randomized, investigator-blinded, multicenter, international, controlled trials. J Am Acad Dermatol. Jul 2008;59(1):41-54. [Medline].
Tey HL, Tan AS, Chan YC. Meta-analysis of randomized, controlled trials comparing griseofulvin and terbinafine in the treatment of tinea capitis. J Am Acad Dermatol. Apr 2011;64(4):663-70. [Medline].
Friedlander SF, Aly R, Krafchik B, et al. Terbinafine in the treatment of Trichophyton tinea capitis: a randomized, double-blind, parallel-group, duration-finding study. Pediatrics. Apr 2002;109(4):602-7. [Medline].
White JM, Higgins EM, Fuller LC. Screening for asymptomatic carriage of Trichophyton tonsurans in household contacts of patients with tinea capitis: results of 209 patients from South London. J Eur Acad Dermatol Venereol. Sep 2007;21(8):1061-4. [Medline].
Pomeranz AJ, Sabnis SS, McGrath GJ, Esterly NB. Asymptomatic dermatophyte carriers in the households of children with tinea capitis. Arch Pediatr Adolesc Med. May 1999;153(5):483-6. [Medline].
Williams JV, Honig PJ, McGinley KJ, Leyden JJ. Semiquantitative study of tinea capitis and the asymptomatic carrier state in inner-city school children. Pediatrics. Aug 1995;96(2 Pt 1):265-7. [Medline].
Arenas R, Toussaint S, Isa-Isa R. Kerion and dermatophytic granuloma. Mycological and histopathological findings in 19 children with inflammatory tinea capitis of the scalp. Int J Dermatol. Mar 2006;45(3):215-9. [Medline].
Elewski BE. Tinea capitis: a current perspective. J Am Acad Dermatol. Jan 2000;42(1 Pt 1):1-20; quiz 21-4. [Medline].
Elewski BE. Cutaneous fungal infections. In: Topics in Dermatology. Tokyo, Japan: Igaku-Shoin; 1992.
Elewski BE. Treatment of tinea capitis: beyond griseofulvin. J Am Acad Dermatol. Jun 1999;40(6 Pt 2):S27-30. [Medline].
Ergin S, Ergin C, Erdogan BS, Kaleli I, Evliyaoglu D. An experience from an outbreak of tinea capitis gladiatorum due to Trichophyton tonsurans. Clin Exp Dermatol. Mar 2006;31(2):212-4. [Medline].
Gorbach SL, Bartlett JG, Zorab R, Blacklow NR , eds. Dermatophyte infections of the hair, tinea capitis in fungal infections of the skin. In: Infectious Diseases. 2nd ed. Philadelphia, Pa: WB Saunders; 1997:1276-95.
Hay RJ. Clinical manifestations and management of superficial fungal infection in the compromised patient. In: Warnock DW, Richardson MD, eds. Fungal Infection in the Compromised Patient. New York, NY: John Wiley & Sons; 1992.
Kwon-Chung KJ, Bennett JE. Medical Mycology. Philadelphia, Pa: Lea & Febiger; 1992.
[Guideline] MacKenzie DWR, Loeffler W, Mantovani A, Fujikura T. Guidelines for the diagnosis, prevention and control of dermatophytosis in man and animals. World Health Organization WHO/CDS/VPH/86.67. 1986.
Mandell GL, Bennett JE, Dolin R, eds. Tinea capitis in dermatophytosis and other superficial mycosis. In: Principles and Practice of Infectious Disease. 1995. New York, NY: Churchill Livingstone; 2379-82.
Richardson MD, Warnock DW. Fungal Infection: Diagnosis and Management. London, England: Blackwell Scientific; 1993.
Rippon JW. Medical Mycology. 3rd ed. Philadelphia, Pa: WB Saunders; 1988.
Rippon JW. Tinea capitis in dermatophytosis and dermatomycosis. In: Medical Mycology, the Pathogenic Fungi and the Pathogenic Actinomycetes. Philadelphia, Pa: WB Saunders; 1988:186-96.
Rook A, Dawber R. Ringworm of the scalp. In: Infections and Infestations: Diseases of the Hair and Scalp. London, England: Blackwell Science; 1982:367-85.
Smith ML. Tinea capitis. Pediatr Ann. Feb 1996;25(2):101-5. [Medline].
Stein DH. Tineas--superficial dermatophyte infections. Pediatr Rev. Nov 1998;19(11):368-72. [Medline].
Yau-Chin Lu. Tinea capitis. In: Skin Diseases in Chinese. Taipei, Taiwan: Medicine Today; 1981:203-6.

