The dermatophytes are a group of fungi that invade and grow in the dead keratin of skin, hair, and nails. Dermatophytes are, by far, the most prevalent of the 3 major classes of superficial infections.[1] Less frequently, superficial skin infections are caused by nondermatophyte fungi (eg, Malassezia furfur in tinea versicolor) and Candida species.
Several species of dermatophytes commonly invade human keratin, and these belong to the Epidermophyton, Microsporum, and Trichophyton genera. They tend to grow outwards on skin, producing a ringlike pattern, hence the term "ringworm". They are very common and affect different parts of the body. Clinically, dermatophytosis infections, also known as tinea, are classified according to the body regions involved.
The type and severity of the host response is often related to the species and strain of the dermatophyte causing the infection. The dermatophytes are the only fungi that have evolved a dependency on human or animal infection for the survival and dissemination of their species. The infection may spread from person to person (anthropophilic), animal to person (zoophilic), or soil to person (geophilic). The most common of these organisms are Trichophyton rubrum, Trichophyton tonsurans, Trichophyton interdigitale and/or Trichophyton mentagrophytes, Microsporum canis, and Epidermophyton floccosum.
Table. Ecology of Common Human Dermatophyte Species. Table reprinted with permission from David Ellis, Bsc (Hons), MSc, PhD, FASM, FRCPA (Hon), Affiliate Associate Professor, The University of Adelaide (http://www.mycology.adelaide.edu.au/mycoses/cutaneous/dermatophytosis).
Dermatophytes are keratinophilic fungi and have the ability to invade keratinized tissue (eg, hair, nails, any area of the skin). They invade, infect, and persist in the stratum corneum of the epidermis and rarely penetrate below the surface of the epidermis and its appendages. Humid or moist skin provides a very favorable environment for the establishment of fungal infection. At a minimum, the skin responds to the irritation of the superficial infection by increased proliferation in the basal cell layer, which causes scaling and epidermal thickening. Clinically, tinea infections are classified according to the body region involved/infected, as follows:
Tinea capitis - Scalp (see the image below)
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Tinea capitis; gray patch ringworm. Gray patch refers to the scaling with lack of inflammation, as noted in this patient. Hairs in the involved areas ....
Tinea manuum and tinea pedis - Palms, soles, and interdigital webs
Tinea corporis - Body (shown in the image below)
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Annular plaque (tinea corporis).
Tinea cruris - Groin
Tinea barbae - Beard area and neck (shown in the image below)
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Wax model of kerionlike tinea barbae. Courtesy of the Museum of the Department of Dermatology, University of Medicine, Wroclaw, Poland.
Tinea faciale - Face
Tinea unguium (onychomycosis) - Nail
Tinea capitis (caused by the species of genera Trichophyton and Microsporum) is the most common pediatric dermatophyte infection. The age predilection is believed to result from the lack of certain florae and fungistatic sebum in this age group. It usually takes 2 weeks to produce clinically visible changes. The natural course of tinea capitis is of a spontaneous cure at puberty, once sebum production begins. Hair invasion is divided into several types. The site of formation of spore-forming bodies classifies the species causing the invasion, as follows:
Ectothrix species: Conidia form on the exterior of the hair shaft; the cuticle is destroyed and involved areas fluoresce a green-yellow under a Wood lamp; this is caused by M canis, Microsporum distortum, M ferrugineum, M audouinii, as well as nonfluorescent T rubrum, T verrucosum, Trichophyton megninii, T mentagrophytes, M gypseum, and M nanum
Endothrix species: Conidia form within the hair shaft, and each is filled with hyphae and spores; the cuticle is not affected, and hairs do not fluoresce under a Wood lamp; this is caused by anthropophilic (T rubrum, Trichophyton gourvilii, T tonsurans, T violaceum, Trichophyton yaoundei, T soudanense) organisms
Favus species: Hyphae arrange within and around the hair shaft; this is a rare and severe form resulting in favuslike crusts or scutula and hair loss with honey comb destruction pattern of the follicles; this is caused by T schoenleinii (see the image below)
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Tinea favosa of the scalp shows erythematous lesions with pityroid scaling. Some hairs are short and brittle.
Kerion: Thick plaques and boggy skin that form often with bacterial infection superimposed; mainly caused by M canis[2] ; this pattern develops in such a manner that it is often believed to be a response to the dermatophyte (see the image below)
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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 ....
The specific etiologic agent is often associated with a specific region of infection. Further elaboration of the discussion below can be found in the tinea articles of the Medscape Reference Dermatology volume (Tinea Barbae, Tinea Capitis, Tinea Corporis, Tinea Cruris, Tinea Faciei, Tinea Nigra, Tinea Pedis, Tinea Versicolor).
A recent study found tinea capitis present in more than 30% of children at certain grade levels in some urban areas of the United States.[3]
High prevalence rates of tinea pedis and onychomycosis have been linked to increased urbanization, community showers, sports, and the use of occlusive footwear.[4] These factors are thought to contribute to the high prevalence of tinea pedis in certain occupational groups, including marathon runners (22-31% prevalence), miners (21-72.9% prevalence), and soldiers (16.4-58% prevalence). Several of these studies also found high rates of onychomycosis presenting with tinea pedis. Outbreaks of infections can occur in schools, households, and institutional settings.
International
Although dermatophytes are found throughout the world, the most prevalent strains and the most common sites of infection vary by region. Hot, humid climates and overcrowding predispose populations to skin diseases, including tinea infections. Developing countries have high rates of tinea capitis, while developed countries have high rates of tinea pedis and onychomycosis.
Low socioeconomic conditions are strongly linked to higher prevalence rates for skin infections, including tinea infections. A review of 18 studies representing large geographical areas determined that tinea capitis is present in up to 19.7% of the general population in developing countries.
Mortality/Morbidity
While mortality due to dermatophytes is very low, there is significant morbidity associated with these infections, particularly in the armed forces and active adults.
Cellulitis in the lower extremities, which causes a breach in the skin and allows the inoculation of opportunistic bacteria, is a frequent complication of interdigital fungal infection.
In patients with impaired cell-mediated immune function, atypical and locally aggressive presentations of dermatophyte infection may occur. These include extensive skin disease, subcutaneous abscesses, and dissemination.
Race
Fungal infection affects all races; however, the prevalence of organisms varies by country.
Sex
Both sexes are affected by fungal infection. Tinea cruris is much more common in males because of the male anatomy, which allows moisture to accumulate in the crural folds.
Age
In the United States, tinea pedis is the most common in adults and tinea capitis is the most common in children. Tinea corporis is present in all ages, although it is more frequent in adolescents and pregnant females.
For excellent patient education resources, visit eMedicineHealth's Skin Conditions and Beauty Center. Also, see eMedicineHealth's patient education articles Ringworm on Body and Ringworm on Scalp.
About 2 weeks elapse from inoculation to subsequent clinically visible skin changes. Tinea pedis often follow activities that cause the feet to sweat.
Pruritus (itching) is the main symptom in most forms of tinea. Findings can be subtle and care must be taken in examination, as a novel form of delusional tinea has been described in several reports.[5] Patients with tinea capitis have hair loss. Infected hairs are brittle and break easily.
Asking the patient about participation in sports, such as judo, karate, wrestling, and other contact sports, is important. Likewise, asking the patient about military enrollment and any contacts with similar skin disease is important.
Tinea corporis can be seen in adults caring for children with tinea capitis.
At physical examination, the various types of tinea may have different findings, as follows:
Tinea capitis: The clinical appearance of fungal infection of the scalp varies depending on the type of hair invasion. Patients typically present with scaling of the scalp or circumscribed alopecia with broken hair at the scalp.
Tinea corporis: Infection is usually on the exposed skin of the trunk and extremities. It is characterized by annular scaly plaques with raised edges, pustules, and vesicles. It can also have geometric patterns. This is usually tinea imbricata (T concentricum). Tinea corporis gladiatorum is seen on the head, neck, and arms, in a distribution consistent with the areas of skin-to-skin contact in wrestling.
Tinea pedis: This is a fungal infection of the toe webs and plantar surface and often affects only one foot. Toe-web scaling, fissuring, and maceration; scaling of soles and lateral surfaces; erythema; vesicles; pustules; and bullae may be present.
Tinea manuum: This is a fungal infection of the palms and finger webs that usually occurs in association with tinea pedis. Similarly, often only one hand is involved. Scaling and erythema may be present.
Tinea cruris: It is a dermatophytic infection of the groin and pubic region. It is characterized by erythematous lesions with central clearing and raised borders. Tinea cruris often co-occurs with tinea pedis or tinea unguium.
Tinea barbae: The beard and neck area are affected. Erythema, scaling, and pustules are present.
Tinea unguium: Tinea unguium is also called onychomycosis. This is an infection of the nail. It is characterized by onycholysis (nail plate separation from nail bed) and thickened, discolored (white, yellow, brown, black), broken, and dystrophic nails.
Tinea incognito: This is a common difficult diagnosis to make without history. It is often present as a result of prior treatment with hydrocortisone, causing atypical appearance.[6]
Autoeczematization reactions: (also known as id reactions) are secondary dermatitic eruptions that occur in association with primary, often inflammatory, skin disorders. It is secondary to a tinea infection at another site. It is due to cell-mediated immunity and resolves with treatment of tinea.
The various tinea infections are caused chiefly by species of the genera Microsporum, Trichophyton, and Epidermophyton. Risk factors for tinea infection include the following:
Moist conditions
Communal baths
Immunocompromised states (including the use of immunosuppressive drugs)
Atopy
Genetic predisposition
Athletic activity that causes skin tears, abrasions, or trauma such as wrestling, judo, or soccer
Direct microscopic examination may be performed. Skin scrapings, nail specimens, or plucked hairs are treated with potassium hydroxide and examined. Hyphae can be visualized in skin and nails. Spores within or around the hair shaft can be detected.
Fungal cultures can be performed for precise identification of the species.
Wood light (UV light) examination may be performed. This examination is used mainly for the diagnosis of tinea capitis. Hairs infected with M audouinii and M canis produce a brilliant yellow-green fluorescence. T schoenleinii causes a dull green fluorescence.
Histology is not needed, but biopsy findings would show spongiosis, parakeratosis (that may alter with orthokeratosis), and a superficial inflammatory infiltrate. Neutrophils may be seen in the stratum corneum, which is a significant diagnostic clue. On occasion, septate branching hyphae are seen in the stratum corneum. Special fungal stains (eg, periodic acid-Schiff, Gomori methenamine silver) may be required.
A biopsy may be needed in recalcitrant or atypical disease.
As mentioned above, dermatophyte infection occasionally leads to formation of a kerion, which is a boggy, large, inflammatory scalp mass caused by a severe inflammatory reaction to the dermatophyte. A kerion may result in scarring hair loss. A kerion may also have pustules and crusting and is commonly mistaken for an abscess. It is important to recognize a kerion because incision and drainage is not indicated. Therefore, other than a biopsy or culture that may be taken by an experienced dermatologist, no procedure is commonly performed by the emergency department physician.[7]
Certain forms of tinea can easily be identified and treated with antifungals in the emergency department. However, the diagnosis should probably be confirmed with a potassium hydroxide smear and/or cultures.
A common practice that is highly discouraged is the prescribing of combined steroid/antifungal creams.
It is important that the evaluating physician be aware of the possible presence of superinfection. This is known as the dermatophytosis complex. In the dermatophytosis complex presentation, inflammation, maceration, and odor may be present with bacterial involvement.
It is imperative to also recognize comorbidities that may increase the healing time or depress host immune response. These comorbidities may include age, diabetes, or immunodeficient status (eg, HIV infection or chronic immunosuppressive use). Defining the relationship between comorbidities and dermatophytosis is complex, since complications of these conditions in themselves, including peripheral vascular disease, could also contribute to persistent infection.
A dermatologist may be consulted. Outpatient phototherapy protocols have been developed for chronic situations in which oral medications are not tolerated.
Tinea corporis infections may be treated with topical agents (ie, creams, lotions, solutions, powders, sprays) as the drug of choice or with oral antifungals in extensive or recalcitrant disease.[8, 9]
For tinea capitis and nail infections, topical therapy is ineffective. Findings with onychomycosis treatment were discouraging because of the need for prolonged therapy and the low success rate. However, in recent years, new oral antimycotic drugs have been developed as the drug of choice; these have greatly improved the outlook (especially for patients with fungal toenail infection).[10, 11, 12]
Use of oral medications requires baseline liver function testing and repeat laboratory testing half way through the typical 3-month course. Cultures are also recommended when managing children, as oral medications are more difficult for this age group.[13]
Medication classes
Two classes of antifungal medications are most commonly used: azoles and the allylamines. Both classes have the common endpoint if inhibiting ergosterol production.
Azoles inhibit lanosterol 14-alpha-demethylase, an enzyme that converts lanosterol to ergosterol (important for the fungal cell wall). This leads to permeability and renders the fungus unable to reproduce.
Allylamines inhibit squalene epoxidase, an enzyme that converts squalene to ergosterol, leading to the accumulation of toxic levels of squalene in the cell and cell death.
Clinical Context:
Imidazole, broad-spectrum antifungal agent indicated for the topical treatment of tinea corporis, tinea cruris, and tinea pedis. Inhibits synthesis of ergosterol (main sterol of fungal cell membranes), causing cellular components to leak; results is cell death.
Clinical Context:
Effective in cutaneous infections. Interferes with RNA and protein synthesis and lipid metabolism. Disrupts fungal cell-wall membrane permeability, causing fungal cell death.
Clinical Context:
Damages fungal cell-wall membrane by inhibiting biosynthesis of ergosterol. Membrane permeability is increased, causing nutrients to leak and resulting in fungal-cell death. The lotion is preferred in intertriginous areas. If the cream is used, apply sparingly to avoid maceration effects.
Clinical Context:
Synthetic allylamine derivative that inhibits squalene epoxidase, a key enzyme in sterol biosynthesis of fungi, resulting in a deficiency in ergosterol that causes fungal cell death. Use until symptoms significantly improve.
Clinical Context:
Indicated for the treatment of tinea corporis, tinea cruris, and tinea pedis. Broad-spectrum antifungal agent that appears to interfere with sterol biosynthesis by inhibiting the enzyme squalene 2,3-epoxidase. This inhibition results in decreased amounts of sterols, causing cell death. If no clinical improvement occurs after 4 weeks of treatment, reevaluate the patient.
Clinical Context:
Extensively used in the past to treat dermatophytic infections of the skin. However, with new antifungals now available, use is now limited. An antibiotic derived from a species of Penicillium that is deposited in the keratin precursor cells, which are gradually replaced by noninfected tissue; the new keratin then becomes highly resistant to fungal invasions. Most used therapy for treating tinea capitis, especially if caused by M canis.
Clinical Context:
Synthetic triazole antifungal agent that inhibits fungal cell growth by inhibiting the cytochrome P-450–dependent synthesis of ergosterol, a vital component of fungal cell membranes.
A 30-d course of 100 mg of itraconazole daily has been shown to effectively treat tinea capitis. This treatment could prove to be a beneficial alternative to griseofulvin therapy.
Clinical Context:
Broad-spectrum triazole antifungal agent. A potent and selective inhibitor of fungal enzymes necessary for ergosterol synthesis. Most commonly used in the treatment of candidiasis.
Clinical Context:
Topical imidazole antifungal active against T rubrum, T mentagrophytes, E floccosum. Indicated for tinea pedis. Inhibits fungal cell growth by inhibiting cytochrome P-450–dependent synthesis of ergosterol, a vital component of fungal cell membranes. Alters fungal cell wall membrane permeability.
The optimal duration of topical therapy for dermatophytic infections of the skin has never been established.[14] In most cases of tinea corporis and tinea cruris, 2 weeks of treatment may suffice. Tinea pedis may require treatment for as long as 8 weeks.
What are tinea infections?What is the pathophysiology of tinea infections?What is the pathophysiology of tinea capitis?What is the prevalence of tinea infections in the US?What is the global prevalence of tinea infections?What is the morbidity of tinea infections?What are the racial predilections of tinea infections?What are the sexual predilections of tinea infections?Which age groups have the highest prevalence of tinea infections?What is the prognosis of tinea infections?Which clinical history findings are characteristic of tinea infections?Which physical findings are characteristic of tinea infections?What are the risk factors for tinea infections?What are the possible complications of tinea infections?What are the differential diagnoses for Tinea in Emergency Medicine?What is the role of lab testing in the workup of tinea infections?What is the role of biopsy in the diagnosis of tinea infections?What is included in emergency department (ED) care for tinea infections?Which specialist consultations are beneficial to patients with tinea infections?How are tinea infections prevented?What is the role of drug treatment for tinea infections?Which antifungal medications are used in the treatment of tinea infections?Which medications in the drug class Antifungals are used in the treatment of Tinea in Emergency Medicine?
Shari Andrews, MD, Attending Faculty, Department of Emergency Medicine, North Shore-Long Island Jewish Medical Center, Hofstra University School of Medicine
Disclosure: Nothing to disclose.
Coauthor(s)
Mityanand Ramnarine, MD, FACEP, Assistant Professor of Emergency Medicine, Associate Chair, Department of Emergency Medicine, Program Director, Emergency/Internal Medicine/Critical Care, Hofstra Northwell School of Medicine at Hofstra University; Attending Physician, Department of Emergency Medicine, Long Island Jewish Medical Center
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Eddy S Lang, MDCM, CCFP(EM), CSPQ, Associate Professor, Senior Researcher, Division of Emergency Medicine, Department of Family Medicine, University of Calgary Faculty of Medicine; Assistant Professor, Department of Family Medicine, McGill University Faculty of Medicine, Canada
Disclosure: Nothing to disclose.
Chief Editor
Jeter (Jay) Pritchard Taylor, III, MD, Assistant Professor, Department of Surgery, University of South Carolina School of Medicine; Attending Physician, Clinical Instructor, Compliance Officer, Department of Emergency Medicine, Palmetto Richland Hospital
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Employed contractor - Chief Editor for Medscape.
Additional Contributors
Theodore J Gaeta, DO, MPH, FACEP, Clinical Associate Professor, Department of Emergency Medicine, Weill Cornell Medical College; Vice Chairman and Program Director of Emergency Medicine Residency Program, Department of Emergency Medicine, New York Methodist Hospital; Academic Chair, Adjunct Professor, Department of Emergency Medicine, St George's University School of Medicine
Disclosure: Nothing to disclose.
Acknowledgements
Andrew C Miller, MD Fellow, Critical Care Medicine Department, National Institutes of Health; Fellow, Department of Pulmonary, Allergy, and Critical Care Medicine, University of Pittsburgh Medical Center
Andrew C Miller, MD is a member of the following medical societies: American College of Emergency Physicians and Society of Critical Care Medicine (USA)
Disclosure: Nothing to disclose.
Rashid M Rashid, MD, PhD Medical Director, Department of Hair Transplants and Dermatology, Mosaic Clinic and Morzak Research Initiative
Rashid M Rashid, MD, PhD is a member of the following medical societies: American Academy of Dermatology, Council for Nail Disorders, Houston Dermatological Society, Texas Dermatological Society, and Texas Medical Association
Disclosure: Nothing to disclose.
Mark A Silverberg, MD, MMB, FACEP Assistant Professor, Associate Residency Director, Department of Emergency Medicine, State University of New York Downstate College of Medicine; Consulting Staff, Department of Emergency Medicine, Staten Island University Hospital, Kings County Hospital, University Hospital, State University of New York Downstate Medical Center
Mark A Silverberg, MD, MMB, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Council of Emergency Medicine Residency Directors, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
References
Cohn MS. Superficial fungal infections: topical and oral treatment of common types. Postgrad Med. 1992. 91:239-52.
Tinea capitis; gray patch ringworm. 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 and are broken and shorter.
Annular plaque (tinea corporis).
Wax model of kerionlike tinea barbae. Courtesy of the Museum of the Department of Dermatology, University of Medicine, Wroclaw, Poland.
Tinea favosa of the scalp shows erythematous lesions with pityroid scaling. Some hairs are short and brittle.
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.
Wax model of kerionlike tinea barbae. Courtesy of the Museum of the Department of Dermatology, University of Medicine, Wroclaw, Poland.
Tinea capitis; gray patch ringworm. 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 and are broken and shorter.
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.
Annular plaque (tinea corporis).
Tinea favosa of the scalp shows erythematous lesions with pityroid scaling. Some hairs are short and brittle.