Tinea Capitis
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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]
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.
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.
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.
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.
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.
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.
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]
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.
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 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.”
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Marc Zachary Handler, MD Fellow in Mohs Micrographic Surgery, Skin Laser and Surgery Specialists of NY and NJ
Marc Zachary Handler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, European Society for Pediatric Dermatology, International Society of Dermatology, New York Academy of Medicine, Sigma Xi, Society for Pediatric Dermatology
Disclosure: Nothing to disclose.
Matthew P Stephany University of Nebraska College of Medicine
Matthew P Stephany is a member of the following medical societies: American Medical Association
Disclosure: Nothing to disclose.
Robert A Schwartz, MD, MPH Professor and Head of Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, Rutgers New Jersey Medical School; Visiting Professor, Rutgers University School of Public Affairs and Administration
Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, New York Academy of Medicine, American Academy of Dermatology, American College of Physicians, Sigma Xi
Disclosure: Nothing to disclose.
Michael J Wells, MD, FAAD Dermatologic/Mohs Surgeon, The Surgery Center at Plano Dermatology
Michael J Wells, MD, FAAD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Texas Medical Association
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
Paul Krusinski, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, Society for Investigative Dermatology
Disclosure: Nothing to disclose.
Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.
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
Grace F Kao, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, International Society of Dermatopathology
Disclosure: Nothing to disclose.
Franklin Flowers, MD Department of Dermatology, Professor Emeritus Affiliate Associate Professor of Pathology, University of Florida College of Medicine
Franklin Flowers, MD is a member of the following medical societies: American College of Mohs Surgery
Disclosure: Nothing to disclose.
Tinea Capitis
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