Author
Dina Strachan, MD
Assistant Clinical Professor of Dermatology, Columbia University College of Physicians and Surgeons
Director, Aglow Dermatology
New York, NY
Disclosure: Dina Strachan, MD, has disclosed no relevant financial relationships.
Editor
Lars Grimm, MD, MHS
House Staff
Department of Internal Medicine
Duke University Medical Center
Durham, North Carolina
Disclosure: Lars Grimm, MD, MHS, has disclosed no relevant financial relationships.
Reviewer
Robert A. Schwartz, MD
Professor and Head, Dermatology
Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health
UMDNJ-New Jersey Medical School
Newark, New Jersey
Disclosure: Robert A. Schwartz, MD, has disclosed no relevant financial relationships.
Tinea is a protean group of fungal infections that can affect the superficial human body from head to toe. The anatomic overlap and confusing nomenclature can make it difficult to confidently identify which disease process is responsible. Separating tinea capitis from tinea favosa, differentiating tinea corporis (shown) from tinea imbricata, and distinguishing tinea faciei from tinea barbae, to name a few, can confound even the most astute diagnostician.
Tinea versicolor is caused by a yeast, of the genus Malassezia, rather than a dermatophyte. This yeast may be part of normal, human flora, in addition to being an opportunistic organism. Affected patients may develop hyperpigmented (left image), hypopigmented (right image), or erythematous scaly macules and patches on the involved areas, commonly on the chest and back. However, the neck, face, and folds may also be affected. Areas of increased sebaceous activity are more at risk. It most commonly occurs in warm, humid environments. Most cases are in healthy individuals without any immunologic deficiencies. It is unclear why this yeast remains a part of the normal flora in some individuals but causes skin changes in others.
The diagnosis of tinea versicolor is usually made based on clinical grounds. However, under potassium hydroxide (KOH) preparation, hyphae (thick strands) and grape-like clumps of spores can be seen, often referred to as "spaghetti and meatballs." Special media are required for culture, which is rarely performed. Oral and topical antifungals are both effective in treating this condition. However, patients should be advised that postinflammatory pigmentary alteration may linger for months after the infection has cleared. Some patients will have recurrent episodes despite adequate treatment.
Dermatophyte infection of the scalp, hair, eyebrows, and eyelashes, known as tinea capitis, is the most common pediatric dermatophyte infection worldwide and is usually seen in preadolescent children. In the United States, tinea capitis is more commonly found in the African American population. Trichophyton tonsurans is responsible for more than 90% of the cases in the United States, resulting in gray patch tinea capitis characterized by scaly, circular patches in the scalp with hair loss (shown). Sporadic infection with zoophilic organisms, such as Microsporum canis, ironically more commonly acquired from cats than dogs, results in a more inflammatory infection.
Differentiating the etiologic agent of tinea capitis can sometimes be made with a Woods lamp examination. M canis emits a green fluorescence, whereas T tonsurans does not. Treatment of tinea capitis usually requires systemic antifungal therapy over several weeks. Antifungal shampoos, such as those containing selenium sulfide, may prevent spread by reducing the shedding of infectious spores. Household contacts and playmates should be evaluated and treated accordingly. Asymptomatic carriers can be a source of recurrent infection. Although the differential diagnosis includes atopic dermatitis, psoriasis, and seborrheic dermatitis (which usually occurs after puberty), tinea capitis should be ruled out in any child, particularly if African American, with a scaly scalp condition, especially if accompanied by hair loss.
Tinea favosa is a chronic inflammatory dermatophyte infection usually caused by T schoenleinii. It can be considered a severe form of tinea capitis. It most commonly affects the scalp hair but may also involve the glabrous skin and nails. It begins with erythema of the scalp. Then a scutula forms with the beginning of hair loss, and finally there are large areas of hair loss with atrophy and scarring (shown). The scutulum is a yellow cup-shaped, dense crust that surrounds a hair follicle. Diagnosis is made with direct microscopy with KOH preparation and fungal culture. Treatment is with systemic antifungals, usually griseofulvin, for a much longer duration than treatment of typical tinea capitis.
Tinea incognito is a dermatophyte infection of the skin (ringworm) that has an altered appearance as a result of the application of the wrong medication -- usually a topical steroid. A classically annular, scaly plaque caused by a tinea infection may spread, become less scaly, take on an unusual shape, or develop pustules or papules. Symptoms of itch may either get better as a result of the antiinflammatory effects of the steroid or get worse. A common presentation is the flaring of the condition with cessation of steroid use, resulting in a cycle of repeated steroid application. Laboratory diagnosis to look for dermatophytes should be performed in this setting. Topical or oral antifungal medications are the treatment of choice.
Tinea corporis is a superficial fungal infection of the skin caused by 1 of 3 species of dermatophytes, Trichophyton (most commonly T rubrum), Microsporum, and Epidermophyton. The etiologic fungus proliferates in a warm, moist environment and is more commonly seen in people residing in hot, humid climates. Lesions are usually erythematous, scaly, annular plaques with an advancing border of scale. Pruritus may or may not be associated with this condition. Immunocompromised patients, such as those infected with HIV, and diabetics tend to have more severe lesions. The infection may be acquired from infected humans, fomites, or animals.
Tinea imbricata, also known as Tokelau, is a concentric, lamellar variant of tinea corporis limited in geographic distribution to areas of the South Pacific, India, and Central America and is caused by T concentricum. The condition may be confused with syphilis, granuloma annulare, and erythema annulare centrifugum. Male children and adult women, particularly pregnant women, are more commonly affected. Some evidence suggests that malnutrition may contribute to an increased incidence of infection. Griseofulvin or terbinafine are the treatments of choice. However, recurrence rates are high. Image courtesy of Wikimedia Commons.
Tinea faciei is a dermatophyte infection of the glabrous skin of the face. It may occur on any surface of the face and is known as tinea barbae when it occurs on the bearded areas in men. Tinea faciei is frequently acquired from pets in the home. It is typically caused by M canis. It may be confused with allergic contact dermatitis or cutaneous lupus erythematosus. The presentations of tinea faciei vary but usually entail erythematous, scaling patches with papules, vesicles, or crusts that are pruritic. The cheeks are most commonly involved. Direct microscopic examination for fungal elements in a KOH preparation is diagnostic. Treatment with topical agents is usually successful, with oral agents reserved for cases of fungal folliculitis.
Tinea barbae is a dermatophyte infection of the bearded area of the face, chin, and neck. It predominantly affects adolescent boys and adult men. The 2 major clinical variants include a noninflammatory form, which can be chronic without treatment, and an inflammatory form, which exhibits indurated plaques and nodules. Inflammatory tinea barbae is commonly acquired from animals. Infected farm workers should have all animals examined. Autoinoculation from nails and feet should also be considered as a cause of infection. Noninflammatory lesions are chronic and usually require oral therapy. Inflammatory lesions may resolve spontaneously with resultant scarring.
Tinea nigra is a rare, superficial fungal infection of the skin that may raise concern of acral melanoma. It presents as an asymptomatic, pigmented patch, usually on the palms and less commonly on the soles. Inoculation with Hortaea werneckii, the causative organism, occurs as a result of skin trauma and contact with contaminated soil, wood, compost, or sewage. Most cases occur in tropical, humid climates. Hyperhidrosis is also a risk factor. The accumulation of a melanin-like substance in the fungus is responsible for the brown color. Diagnosis can be made with KOH preparation or fungal culture. Treatment includes topical keratolytic agents, such as salicylic acid and tretinoin, as well as antifungals.
Dermatophyte infection of the nails is the most common cause of nail dystrophy, affecting the nails on the toes more commonly than nails on the fingers. Infection usually occurs as the result of spread from the surrounding skin, resulting in a thickened, opaque, yellowed appearance in the nail. Risk factors for tinea unguium include a family history, occlusive footwear, participation in athletics, diabetes mellitus, and an immunocompromised state. Diagnosis requires confirmation of the presence of dermatophytes by KOH preparation, culture, or histology because conditions, such as psoriasis and trauma, may also produce similar changes in the appearance of the nails.
Standard treatments for tinea unguium include oral antifungals, which seem to be the most effective; topical lacquers; and debridement. Combination therapy has been shown to be superior to any single agent. Laser treatments and topical botanical treatments have also been shown to be effective, but the efficacy of these modalities needs more scientific support. Image courtesy of Dr. Antonella Tosti.
Tinea pedis affects the soles and interdigital spaces of the feet. Fungal proliferation is assisted by the humid environment created by occlusive footwear. The causative agents are most commonly T rubrum (most frequent), T mentagrophytes, and Epidermophyton floccosum. Although rare before puberty, T tonsurans may be the cause in children. Men are more commonly affected than women. Trauma, host immune factors, and species of invading organism are also thought to contribute to susceptibility to infection. There are a variety of clinical variants, including interdigital (usually affecting the 4th interdigital web space), hyperkeratotic, and vesicular.
Compromise of the skin barrier as a result of tinea pedis can be the set up for a bacterial superinfection, resulting in cellulitis, especially in diabetic and immunocompromised patients. Tinea pedis may be treated with a variety of topical and oral antifungal medications. However, avoiding occlusive footwear, protecting feet in public places, and discarding or treating infected shoes may be helpful to prevent reinfection. Keratolytics may be necessary when thick scale is present.
Tinea cruris is a superficial fungal infection of the groin and adjacent skin. It is the second most common clinical presentation for dermatophytosis. The most common etiologic agents are T rubrum and E floccosum. Tinea cruris is a contagious infection transmitted by fomites, such as contaminated towels or hotel bedroom sheets, or by autoinoculation from the hands or feet. On examination, patients will have a symmetric erythematous rash in the groin (shown), centered on the inguinal creases that extend distally down the medial thighs and proximally to the lower abdomen.
The diagnosis of tinea cruris can usually be made on the basis of the distribution of the rash. Typically, the penis and scrotum are spared, but the perineum and buttocks may be involved. KOH wet mount examination can be performed to exclude other conditions. Treatment with topical antifungal agents is usually effective. All active areas of fungal infection, including the hands and feet, must be treated simultaneously. Otherwise, reinfection will occur. Patients are advised to use separate towels for drying the groin from other parts of the body.
Author
Dina Strachan, MD
Assistant Clinical Professor of Dermatology, Columbia University College of Physicians and Surgeons
Director, Aglow Dermatology
New York, NY
Disclosure: Dina Strachan, MD, has disclosed no relevant financial relationships.
Editor
Lars Grimm, MD, MHS
House Staff
Department of Internal Medicine
Duke University Medical Center
Durham, North Carolina
Disclosure: Lars Grimm, MD, MHS, has disclosed no relevant financial relationships.
Reviewer
Robert A. Schwartz, MD
Professor and Head, Dermatology
Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health
UMDNJ-New Jersey Medical School
Newark, New Jersey
Disclosure: Robert A. Schwartz, MD, has disclosed no relevant financial relationships.
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