Tinea in Emergency Medicine

Background

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).

View Table

See Table

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Pathophysiology

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).

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Epidemiology

Frequency

United States

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.

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Prognosis

Skin tinea infection generally resolves without sequelae within 1-2 weeks of therapy. Hair and nail tinea require 3-6 months of treatment.

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Patient Education

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.

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History

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.

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Physical

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.

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Causes

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

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Complications

Complications of tinea infection include the following:

• Bacterial superinfection
• Generalized invasive dermatophyte infection

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Laboratory Studies

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.

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Procedures

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]

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Emergency Department Care

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.

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Consultations

A dermatologist may be consulted. Outpatient phototherapy protocols have been developed for chronic situations in which oral medications are not tolerated.

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Prevention

Deterrence and prevention of tinea infection includes the following:

• Practice proper hygiene.
• Avoid contact with suspicious lesions.

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Medication Summary

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.

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Ketoconazole topical (Nizoral, Extina, Ketodan, Xelogel)

• Dosing, Interactions, etc.

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.

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Clotrimazole 1% cream or lotion (Lotrimin AF, Alevazol, Clotrimazole Anti-Fungal, Desenex)

• Dosing, Interactions, etc.

Clinical Context:  Indicated for topical treatment of tinea corporis, tinea cruris, and tinea pedis. Broad-spectrum antifungal agent that inhibits yeast growth by altering cell membrane permeability, causing fungal cell death.

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Econazole topical (Ecoza)

• Dosing, Interactions, etc.

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.

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Miconazole topical (Mikaderm, Micatin, Podactin, Secura Antifungal, DermaFungal)

• Dosing, Interactions, etc.

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.

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Terbinafine (Lamisil)

• Dosing, Interactions, etc.

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.

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Naftifine 1% cream (Naftin)

• Dosing, Interactions, etc.

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.

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Griseofulvin (Gris-PEG, Grifulvin V)

• Dosing, Interactions, etc.

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.

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Itraconazole (Sporanox)

• Dosing, Interactions, etc.

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.

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Fluconazole (Diflucan)

• Dosing, Interactions, etc.

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.

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Sertaconazole nitrate cream (Ertaczo)

• Dosing, Interactions, etc.

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.

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Class Summary

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.

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