Superficial fungal infections

Superficial fungal infections can usually be suspected clinically, but definitive diagnosis requires the demonstration of fungal pathogens by microscopic examination or culture of skin, nail, or hair scrapings from the suspected lesion. During microscopic examination, hyphae are sought in the material. The material is first placed on a glass slide, and then 1 or 2 drops of 10% to 20% potassium hydroxide (KOH) are added. A fungal stain such as chlorazol black E may be added to the preparation to aid visualization of the fungal elements. The hyphae of dermatophytes will be septate and typically demonstrate branching (see Figure 3-1). Skin scrapings can also be placed on culture media. Culturing the organism, in addition to being a diagnostic aid, permits speciation of the organism.

The superficial dermatophyte infections are classified according to their location on the affected person. This location does not necessarily reveal the identity of the offending organism. The infection will cause the production of scale. The scale may or may not be associated with erythema, vesicles, or annular plaques (Table 31-1, Fig. 31-1).

Trichophyton rubrum.

Table 31-1. Clinical Presentations of Dermatophyte Infections

INFECTION	LOCATION
Tinea capitis	Scalp
Tinea faciei (see Fig. 31-1A)	Face
Tinea barbae	Beard
Tinea corporis (see Fig. 31-1B)	Trunk, extremities
Tinea cruris (see Fig. 31-1C)	Groin
Tinea manuum (manus)	Hands
Tinea pedis	Feet
Tinea unguium	Nails

Foster KW, Ghannoum MA, Elewski BE: Epidemiologic surveillance of cutaneous fungal infections in the United States from 1999 to 2002, J Am Acad Dermatol 50:748–752, 2004.

Until the mid-1950s, Microsporum audouinii was the most common cause of endemic tinea capitis in the U.S., but it has since been replaced by Trichophyton tonsurans. Several theories have been proposed to explain the almost total disappearance of M. audouinii from the U.S., but the most plausible theory is that it was eradicated by the widespread use of griseofulvin. At the same time that M. audouinii disappeared, T. tonsurans, formerly an uncommon cause of tinea capitis, quickly spread. This species was probably introduced into the U.S. from Central or South America.

Foster KW, Ghannoum MA, Elewski BE: Epidemiologic surveillance of cutaneous fungal infections in the United States from 1999 to 2002, J Am Acad Dermatol 50:748–752, 2004.

1. The seborrheic pattern has a dandruff-like scaling of the scalp and should be considered in prepubertal children with suspected seborrheic dermatitis (Fig. 31-2A).

2. In the black-dot pattern, hairs are broken off at the skin line, and black dots are seen within the areas of alopecia (Fig. 31-2B). In the U.S., this pattern is primarily associated with T. tonsurans infections.

3. A kerion is an inflammatory fungal infection that may mimic a bacterial folliculitis or an abscess of the scalp (Fig. 31-2C). The scalp is tender to the touch, and the patient usually has posterior cervical lymphadenopathy.

Tinea capitis is one of the most commonly misdiagnosed skin infections. Any prepubertal child who presents with a scaly scalp dermatitis or carries a diagnosis of seborrheic dermatitis should be presumed to have a dermatophyte infection of the scalp until proven otherwise. Similarly, any child who presents with one or more scalp abscesses most likely has a kerion. Kerions are frequently secondarily infected with Staphylococcus aureus, and unsuspecting health care providers often mistakenly treat kerions as bacterial abscesses.

Sobera JO, Elewski BE : Fungal infections. In Bolognia JL, Jorizzo, JL, Rapini RP, et al, editors: Dermatology, New York, 2008, Mosby, pp 1135–1163.

1. Endothrix infections are produced by fungi that invade the inside of the hair shaft and are composed of fungal arthroconidia and hyphae (Fig. 31-3). A helpful mnemonic to remember the organisms that cause endothrix invasion is: “TVs are in houses.”—T is Trichophyton tonsurans, V is violaceum, and S is soudanense.

A Wood’s light is an ultraviolet light source that emits in the spectrum of 325 to 400 nm. This light was used extensively for the diagnosis of tinea capitis when Microsporum audouinii was the major cause of this disorder. However, it is of limited usefulness today because most cases are now produced by Trichophyton tonsurans, which is not fluorescent. The fluorescence is caused by pteridine. The fungi responsible for fluorescent tinea capitis can be remembered by the mnemonic “See Cats and Dogs Fight.”

After the presence of a fungal infection is demonstrated by either culture or a positive KOH smear, treatment with an oral antifungal agent should be instituted. Most patients are placed on griseofulvin. Microsized griseofulvin at a dose of 20 to 25 mg/kg/day should be taken with meals to improve absorption. The medication is continued for 4 to 6 weeks, after which the site is recultured. Using antifungal shampoo may reduce shedding of the organism. Members of the patient’s family also should be evaluated for infection or a carrier state, and treated if needed. Patients who fail to respond to griseofulvin or are intolerant should be treated with an alternative treatment regimen:

A carrier is a person who does not have clinical signs of tinea capitis but has a positive fungal culture from the scalp. In families in whom tinea capitis is identified, the carrier rate in adults is around 30%. The presence of these carriers will reduce the cure rate for tinea capitis if they are not treated concomitantly. Treatment can include shampooing with selenium sulfide or other antifungal shampoo.

Babel D, Baughman S: Evaluation of the adult carrier state in juvenile tinea capitis caused by Trichophyton tonsurans, J Am Acad Dermatol 21:1209–1212, 1989.

Neil G, Hanslo D, Buccimazza S, Kibel M: Control of the carrier state of scalp dermatophytes, Pediatr Infect Dis J 9:57–58, 1990.

Scytalidium dimidiatum has been isolated from cases of moccasin-type pedis that are resistant to standard therapy. The organism will not grow on selective dermatophyte media, such as Mycosel, Mycobiotic, or DTM, but it does grow readily on Sabouraud’s agar.

Hay RJ, Moore MK: Mycology. In Burns T, Breathnach S, Cox N, Griffiths C, editors: Rook’s textbook of dermatology, ed 8, vol 2, Malden, MA, 2010, Blackwell Publishing, pp 31.10–31.14.

Dermatophytid reactions are inflammatory reactions at sites distant from the site of the associated dermatophyte infection. Types of dermatophytid reactions from tinea pedis include urticaria, hand dermatitis (Fig. 31-4), or erythema nodosum. The pathogenesis of dermatophytid reactions is not fully understood, but evidence suggests that they are secondary to a strong host immunologic response against fungal antigens.

1. Distal subungual onychomycosis presents as onycholysis, subungual debris, and discoloration beginning at the hyponychium that spreads proximally. The most common organism is Trichophyton rubrum (Fig. 31-5).

Tinea versicolor (pityriasis versicolor) is a hypopigmented, hyperpigmented, or erythematous macular eruption. Macules may coalesce into large patches with an adherent fine scale (Fig. 31-6). Lesions are located predominantly on the trunk but may extend to the extremities. The proper taxonomic nomenclature of the lipophilic yeast that produces this infection is debatable. Studies indicate Malassezia globosa is the organism most frequently associated with tinea versicolor, although most older references list M. furfur as the most common organism. This eruption begins during adolescence, when the sebaceous glands become active. The eruption tends to flare when the temperatures and humidity are high. Immunosuppression, systemic corticosteroids, and sweaty or greasy skin will also cause this disease to flare.

Erchiga VC, Florencio VD: Malassezia species in skin diseases, Curr Opin Infect Dis 15:133–142, 2002.

Gupta KA, Batra R, Bluhm R, Faergemann J: Pityriasis versicolor, Dermatol Clin 21: 413–429, 2003.

Prohic A, Ozegovic L: Malassezia species isolated from lesional and non-lesional skin in patients with pityriasis versicolor, Mycoses 50:58–63, 2007.

In the past, Malassezi has been suggested to induce hypopigmentation by production of dicarboxylic acid. These compounds do not have a direct effect on melanocytes in tissue culture. The dark lesions of tinea versicolor may be due to a variation in the inflammatory response to the infection. There is not any strong evidence that influences current thought on this question (Fig. 31-7).

Hay RJ, Moore MK: Mycology. In Burns T, Breathnach S, Cox N, Griffiths C, editors: Rook’s textbook of dermatology, ed 8, vol 2, Malden, MA, 2010, Blackwell Publishing, pp 31.10–31.14.

This organism can also produce a folliculitis of the trunk, arms, and neck area. Malassezia folliculitis presents as pruritic follicular papules and pustules that do not respond to antibiotic therapy. The yeast can be demonstrated by skin biopsies or direct examination of purulent material. The severity of seborrheic dermatitis has been reported to be associated with an increase in Malassezia microflora.

Hay RJ, Moore MK: Mycology. In Burns T, Breathnach S, Cox N, Griffiths C, editors: Rook’s textbook of dermatology, ed 8, vol 2, Malden, MA, 2010, Blackwell Publishing, pp 31.10–31.14.

Piedra refers to adherent deposits on the hair shaft caused by superficial fungal infections. Black piedra, which is caused by Piedraia hortae, presents as firm black nodules on the hair shaft. Trichosporon beigelii is the etiologic agent that produces white piedra, which results in the formation of less-adherent white concretions on the hair shaft. This organism has been reclassified into over six pathologic species, with the T. inkin and T. ovoides being the most common causes of white piedra in pubic hair.

Fitzpatrick JE: Superficial fungal skin diseases. In James WD, editor: Textbook of military medicine. Part III. Disease and the environment, Washington, DC, 1994, Office of the Surgeon General at Textbook of Military Medicine Publication, Borden Institute, Walter Reed Medical Center, pp 423–451.

Sobera JO, Elewski BE : Fungal infections. In Bolognia JL, Jorizzo JL, Rapini RP, et al, editors: Dermatology, New York, 2008, Mosby, pp 1135–1163.

The clinical presentations vary with the sites involved, duration of infection, and immune status of the host (Table 31-2). Most sites show erythema, edema, and a thin purulent discharge (Fig. 31-8).

The factors that predispose to the development of candidiasis are both endogenous and exogenous. Exogenous factors include occlusion, moisture, and warm temperature. Endogenous factors can include immunosuppression, diabetes mellitus, other endocrinopathies, antibiotics, oral contraceptives, Down syndrome, malnutrition, and pregnancy.

Table 31-2. Clinical Presentations of Cutaneous Candidiasis

DISEASE	CLINICAL DESCRIPTION
Intertrigo	Superficial pustules, erythema, edema, creamy exudates within skin folds
Thrush	White, adherent, cottage cheeselike plaques on oral mucosa
Perlèche	Erythema, fissuring, creamy exudate at the angles of the mouth
Paronychia	Tender, erythematous, indurated proximal nail fold, with or without a purulent discharge
Erosio interdigitalis blastomycetica	Erythema, fissuring, maceration of the webspaces between the fingers

Wagner D, Sohnle P: Cutaneous defenses against dermatophyte and yeasts, Clin Microbiol Rev 8:317–335, 1995.

Thymoma, myasthenia gravis, myositis, and aplastic anemia have been associated with the development of chronic mucocutaneous candidiasis after the third decade of life.

Hay RJ, Moore MK: Mycology. In Burns T, Breathnach S, Cox N, Griffiths C, editors: Rook’s textbook of dermatology, ed 8, vol 2, Malden, MA, 2010, Blackwell Publishing, pp 31.10–31.14.

See Table 31-3.

Table 31-3. Oral Antifungal Agents

CLASS	EXAMPLES	MECHANISMS OF ACTION
Antibiotic	Griseofulvin	Arrest of cellular division, dysfunction of spindle microtubules
Polyenes	Nyastatin	Binds irreversibly with ergosterol, altering membrane permeability
Azoles	Fluconazole Itraconazole Ketoconazole	Inhibits ergosterol production by inhibiting the cytochrome P-450 lanosterol 14-demethylase
Allyamines	Terbinafine	Blocks ergosterol production by inhibiting squalene epoxidase

Data from Gupta A, Sauder D, Shear N: Antifungal agents: part II, J Am Acad Dermatol 30:911–933, 1993.

Gupta A, Sauder D, Shear N: Antifungal agents: part II, J Am Acad Dermatol 30:911–933, 1993.

Cytochrome P-450 3A4. Fluconazole inhibits this enzyme at doses greater than 200 mg/day. Fluconazole is also a cytochrome 2C9 inhibitor, and it can affect the metabolism of angiotension II inhibitors, oral hypoglycemic agents, and oral anticoagulants.

Gupta AK: Systemic antifungal agents. In Wolverton SE: Comprehensive dermatologic drug therapy, ed 2, Phildelphia, 2007, Saunders Elsevier, pp 75–99.

Katz I, Gupta AK: Oral antifungal drug interactions: a mechanistic approach to understanding their cause, Dematol Clin 21:543–563, 2003.

Venkatakrishnan K, von Moltke LL, Greenblatt DJ: Effects of the antifungal agents on oxidative drug metabolism: clinical relevance, Clin Pharmacokinet 38:111–180, 2003.

Warfarin, quinidine, digoxin, calcium channel blockers, bulsufan, HIV protease inhibitors, cyclosporine, angiotensin II inhibitors, tacrolimus, oral hypoglycemic agents, hydantoin anticonvulsants, and alcohol. These drugs should be used with caution, because the primary effect of azole antifungal drugs on hepatic enzyme metabolism is inhibition. This results in an elevation of the serum level of any drug that requires hepatic metabolism by the cytochrome P-450 3A4 enzyme in order to be removed.

Gupta AK, Ryder JE: The use of oral antifungal agents to treat onychomycosis, Dermatol Clin 21:469–479, 2003.

Griseofulvin is not effective against tinea versicolor or cutaneous candidiasis. Oral nystatin is not absorbed from the gastrointestinal tract. Topical nystatin and amphotericin are both ineffective against dermatophyte infections. Allylamines have limited effectiveness against tinea versicolor and candidiasis.

Lesher J: Therapeutic agents for dermatologic fungal diseases, In Elewski B, editor: Cutaneous fungal infection, ed 2, Malden, MA, 1998, Blackwell Science, pp 321–346.