Superficial Fungal Infections:  The are a group of taxonomically related fungi whose ability to form molecular attachments to keratin and use it as a source of nutrients allows them to colonize keratinized tissues, including the stratum corneum of the epidermis, , nails, and the horny tissues of animals.

 MICROSCOPIC EXAMINATION  Hair Examination of lesions involving the scalp or beard with a Wood lamp may reveal the fluorescent pteridine of certain pathogens .  must be plucked, not cut, for examination by low-power microscopy, which may reveal three possible patterns of infection:

Ectothrix—small or large arthroconidia forming a sheath around the hair shaft —arthroconidia within the hair shaft Favic—hyphae arranged in parallel within and around the hair shaft  Skin and nails Skin samples should be taken by scraping with the dull edge of a scalpel outward from the advancing margins of a lesion.  Nail specimens must include clippings of the entire thickness of dystrophic areas of nail, as proximal from the distal edge as possible.  In a potassium hydroxide (KOH) preparation, fungal hyphae will appear as septate and branching structures ; however, culture is required for speciation.

Microscopic examination of skin scrapings (scales) revealing septate, branching hyphae.

 CULTURE PROCEDURES . Sabouraud's dextrose agar (SDA) [dextrose 40 g; agar 20 g; peptone 10 g; distilled water (adjusted to pH 5.5) to 1000 mL] is the most commonly used isolation medium and serves as the basis for most morphologic descriptions.  Addition of cycloheximide (0.5 g/L) and chloramphenicol (0.05 g/L) to inhibit saprobes and , making the medium highly selective for the isolation of dermatophytes. Commercial versions of this agar are Mycosel and Mycobiotic.  test medium (DTM) contains the pH indicator phenol red; it remains yellow with the growth of most saprophytes, but turns red when dermatophyte proteolytic activity increases the pH to 8 or above.  Cultures are incubated at room temperature (26°C/78.8°F) for up to 4 weeks before being discarded as no growth.  Host variability also affects presentation. Immunocompromised individuals are more susceptible to severe or refractory dermatophytoses .  Age, sex, and race are additional important epidemiologic factors, as dermatophyte infections are five times more prevalent in males than females . Pathogenesis

 They must resist the effects of UV light, variation in temperature and moisture, competition from normal flora, and fungistatic fatty acids and sphingosines produced by keratinocytes.  After adherence, spores must germinate and penetrate the stratum corneum at a rate faster than desquamation.  This penetration is accomplished by the secretion of proteinases, lipases, and mucinolytic enzymes, which also provide nutrients.  Trauma and maceration also facilitate penetration. competition for iron by unsaturated transferrin  progesterone.  Type IV, or delayed-type hypersensitivity (DTH), plays a pivotal role in clearing dermatophytoses. This arm of cellular immunity is maintained by interferon-gamma secretion from type 1 T- helper lymphocytes (T H1 cells).  Atopic individuals are notoriously susceptible to chronic dermatophytosis.  A likely explanation is that atopy, in which overactive type 2 T-helper lymphocytes (T H2 cells) induce IH responses to antigen, inhibits or overpowers the ability of T H1 cells to maintain a DTH response .  Dermatophytid reactions, which occur in 4 to 5 percent of patients, are inflammatory reactions of the skin at a site distant from the primary fungal infection.  Unlike the primary lesion, these are KOH examination and culture negative.  They may take the form of follicular papules, , vesicular id of the hands and feet, -like, erythema annulare centrifugum, or urticarial.

 Genetics  In households afflicted with T. concentricum and T. rubrum, relatives are more likely to be infected than conjugal partners, even with equal exposure to the fungus.  Also, pedigrees from families with chronic dermatophytoses suggest an autosomal dominant pattern of susceptibility.  DERMATOPHYTOSES   Tinea capitis is a dermatophytosis of the scalp and associated hair. It may be caused by any pathogenic dermatophyte except E. floccosum and T. concentricum. The most common cause worldwide is M. canis, whereas in the United States it is T. tonsurans.  PIDEMIOLOGY It is most commonly found in children ages 3 to 14 years; it is uncommon in adults.  Transmission is increased with decreased personal hygiene, overcrowding, and low socioeconomic status .  PATHOGENESIS Ectothrix dermatophytes typically establish infection in the perifollicular stratum corneum, spreading around and into the hair.  The pathogenesis of endothrix infections is the same except that arthroconidia remain within the hair shaft, replacing the intrapilary keratin and leaving the cortex intact.  As a result, the hair is very fragile and breaks at the surface of the scalp where support from the follicular wall is lost, leaving behind a tiny black dot.  Thus, “black dot” tinea capitis is observed. Endothrix infections are also more chronic because of their ability to persist past the anagen phase into the telogen phase.

 Inflammatory type This pattern is usually seen with zoophilic or geophilic pathogens, the most common examples being M. canis and M. gypseum, respectively.  The spectrum of inflammation ranges from a pustular to which is a boggy mass studded with broken hairs and follicular orifices oozing with pus.  Such inflammation often results in scarring alopecia. Inflammatory lesions are usually pruritic, and may be associated with pain, cervical , fever, and additional lesions on glabrous skin.

 “Black dot” tinea capitis This form of tinea capitis is caused by the anthropophilic endothrix organisms T. tonsurans or T. violaceum.  When it does, hairs broken at the level of the scalp leave behind grouped black dots .  Diffuse scaling is again usually present, but inflammation varies from minimal to pustular folliculitis or furuncle-like lesions to kerion.  Affected areas are usually multiple or polygonal with poorly demarcated, finger-like margins. Normal hairs commonly remain within patches of alopecia.

 DIFFERENTIAL DIAGNOSIS The differential diagnosis of minimally inflammatory, scaly tinea capitis includes seborrheic dermatitis, , and . Pronounced alopecia invites the consideration of , trichotillomania, secondary , and pseudopelade.  The hairs of tinea capitis do not display the exclamation point morphology typical of alopecia areata or the artifactual-appearing hairs of different lengths seen with trichotillomania.

 The differential diagnosis of scarring alopecia also includes discoid erythematosus, lichen planopilaris, pseudopelade, and radiation dermatitis.

 TREATMENT Systemic are necessary for clearance of tinea capitis as they penetrate the hair follicle.  Oral griseofulvin has been the gold standard of therapy for the past 40 years, but is being increasingly challenged by simpler regimens of the oral triazole and allylamine antifungals.  Griseofulvin  The pediatric dosage is 10 to 20 mg/kg per day of the ultramicrosize form taken with a fatty meal to facilitate absorption.  Treatment is continued until clinical and mycologic cure is documented, which usually takes 6 to 8 weeks.  The dose may be increased to 20 to 25 mg/kg per day for refractory infections.  The disadvantages of griseofulvin include poor compliance because of cost, length of treatment, its bitter taste in liquid form, photosensitivity, and gastrointestinal side effects.  It also potently induces cytochrome P450 enzymes .  Fluconazole fluconazole at doses of 6 mg/kg per day for 20 days is 89 percent effective in curing T. tonsurans tinea capitis.  Another effective treatment option appears to be once-weekly dosing of 8 mg/kg fluconazole for 8 to 16 weeks.  Absorption of fluconazole is not affected by meals, and gastrointestinal side effects are uncommon.  Hepatitis has been reported, but occurs less frequently than with ketoconazole.

 Itraconazole At doses of 3 to 5 mg/kg per day, itraconazole effectively eradicates tinea capitis caused by either Microsporum or species in 4 to 6 weeks.  Possible adverse effects of itraconazole include gastrointestinal upset, diarrhea with liquid itraconazole, and peripheral edema, especially when used in conjunction with calcium channel blockers.  Like fluconazole, hepatotoxicity occurs at much lower rates than with ketoconazole.  Routine monitoring of hematologic and hepatic function is only necessary for therapy continuing beyond 4 weeks.

 Terbinafine Doses of 3 to 6 mg/kg per day of terbinafine can cure Trichophyton tinea capitis in 2 to 4 weeks, but requires 4 to 8 weeks for treatment of Microsporum.  Terbinafine also produces gastrointestinal side effects and rare hepatitis.  Although it has fewer cytochrome P450 effects than the other oral antifungals, tricyclic antidepressant toxicity has occurred with concomitant terbinafine use as a result of CYP2D6 inhibition.  Hepatic function and a complete blood count need only be monitored for therapy extending beyond 6 weeks.

 Adjuvant therapy With markedly inflammatory tinea capitis, oral glucocorticoids may reduce the incidence of scarring.  The usual dose of prednisone is 1 mg/kg each morning for the first 10 to 15 days of therapy.  Household transmission may be prevented through the treatment of infected family members or animals and disinfection of the environment.  The use of ketoconazole 2% shampoo or selenium sulfide 2.5% by all household members three times weekly also reduces transmission by decreasing the shedding of spores.  Children may attend school during treatment.

 Tinea Favosa  Tinea favosa or (Latin, “honeycomb”) is a chronic dermatophyte infection of the scalp, glabrous skin, and/or nails characterized by thick yellow crusts (scutula) within the hair follicles which lead to scarring alopecia.

 EPIDEMIOLOGY Favus is usually acquired before adolescence and extends into adulthood.  Associated with malnutrition and poor hygiene, it has become geographically limited in the past century, as it is now seen almost exclusively in Africa .  ETIOLOGY T. schoenleinii is the most common cause of human favus .  CLINICAL MANIFESTATIONS  yellow concave crust .  The scutulum may reach 1 cm in diameter.  cheese-like or musky odor.  Over several years the lesions advance peripherally, leaving central, atrophic clearings of alopecia.  Glabrous skin involvement may be papular, papulosquamous, or vesicular, with or without scutula. T. schoenleinii nail invasion is indistinguishable from other causes of .

 LABORATORY FINDINGS T. schoenleinii exhibits subtle grayish green fluorescence along the entire hair with Wood lamp examination.

 DIFFERENTIAL DIAGNOSIS Atypical and early favus may be difficult to distinguish from seborrheic dermatitis, psoriasis, or tinea amiantacea.  With the development of cicatricial alopecia, favus must be differentiated from radiation or chemical injury, pseudopelade, folliculitis decalvans, lupus erythematosus, and lichen planopilaris.

 TREATMENT Griseofulvin (1 g/day of the microcrystalline form or 0.5 g/day of the ultramicrosize version) is effective in the treatment of favus. Concomitant nail infection, however, requires 6 to 12 months of therapy.

 Tinea barbae (tinea sycosis, barber's itch) is a dermatophytosis of the facial terminal hair of men. Dermatophytosis of the same area in females or prepubertal males involves glabrous skin and is termed tinea faciale.  Tinea barbae is now often contracted by direct exposure to cattle, horses, or dogs, and is thus most commonly seen in rural settings on farmers or ranchers.

 Tinea barbae is most commonly caused by the zoophilic organisms T. mentagrophytes and T. verrucosum .  CLINICAL MANIFESTATIONS Tinea barbae is typically unilateral and more often involves the beard area than the moustache or upper lip. Three forms exist: (1) inflammatory or kerion-like, (2) superficial or sycosiform type, and (3) the circinate, spreading type.

 Inflammatory type Usually caused by T. mentagrophytes and T. verrucosum, inflammatory tinea barbae is analogous to kerion formation in tinea capitis. The lesions are nodular and boggy with a crusting seropurulent discharge. Hairs in this area are lusterless, brittle, and easily epilated to demonstrate a purulent mass about the root. Perifollicular pustulation may coalesce to form sinus tracts and -like collections of pus, eventuating in a scarring alopecia.

 Superficial type This form of tinea barbae closely resembles bacterial folliculitis, with diffuse erythema and perifollicular papules and pustules. Hairs that are dull and brittle make endothrix infection .

 Circinate type Much like tinea circinata of glabrous skin, circinate tinea barbae exhibits an active, spreading vesiculopustular border with central scaling and relative sparing of the hair.

 DIFFERENTIAL DIAGNOSIS Other diagnoses to consider with tinea barbae include bacterial folliculitis (sycosis vulgaris), perioral dermatitis, candidal folliculitis, pseudofolliculitis barbae, acneiform dermatitis, , and . Bacterial folliculitis is more often bilateral, more painful, and more commonly involves the upper lip. History, patch testing, Tzanck smears, or viral cultures can identify the other diagnoses.

 TREATMENT Microsize griseofulvin at 1g daily until 2 to 3 weeks after clinical resolution is recommended for tinea barbae, particularly chronic cases. However, inflammatory T. verrucosum, T. mentagrophytes, and M. canis infections usually resolve without treatment in 2 to 4 weeks. Adjunct measures include topical antifungals, warm compresses, shaving, and débridement of crusted discharge. Systemic glucocorticoids are helpful for symptoms of severe inflammatory lesions.

(Tinea Circinata)  Tinea corporis refers to all dermatophytoses of glabrous skin except the palms, soles, and groin.  EPIDEMIOLOGY Tinea corporis may be transmitted directly from infected humans or animals, via fomites, or via autoinoculation from reservoirs such as T. rubrum colonization of the feet. Children are more likely to contract zoophilic pathogens, especially M. canis from dogs or cats.

 The occlusive clothing, frequent skin-to-skin contact, and minor trauma (mat burns) of competitive wrestling create an environment in which dermatophytes flourish.  Numerous outbreaks of “tinea corporis gladiatorum” have resulted, mostly caused by T. tonsurans.  , caused by T. concentricum, is largely limited to areas of the Far East, South Pacific, and South and Central America necessity to acquire chronic infection in early childhood and genetic susceptibility .

 DIFFERENTIAL DIAGNOSIS The differential diagnosis of annular tinea corporis includes erythema annulare centrifugum, nummular eczema, and annulare. consists of intradermal papules without scale. A papulosquamous lesion of tinea corporis may resemble psoriasis, , secondary syphilis, seborrheic dermatitis, , or .  TREATMENT For isolated lesions of tinea corporis, topical agents such as the allylamines, imidazoles, tolnaftate, butenafine, or ciclopirox are effective. Most are applied twice daily for 2 to 4 weeks. Oral antifungals are reserved for widespread or more inflammatory lesions.

 Tinea cruris is a dermatophytosis of the groin, genitalia, pubic area, perineal, and perianal skin.  like tinea corporis, tinea cruris spreads via direct contact or fomites, and is exacerbated by occlusion and warm, moist climates.  Again, autoinfection from distant reservoirs such as tinea pedis caused by T. rubrum or T. mentagrophytes is common.

 ETIOLOGY Most tinea cruris is caused by T. rubrum, T. mentagrophytes, and E. floccosum, with the latter being most often responsible for epidemics.  CLINICAL MANIFESTATIONS Tinea cruris usually appears as multiple erythematous papulovesicles with a well-marginated, raised border.  Pruritus is common, as is pain with maceration or secondary infection.

 The genitalia are typically unaffected.  Common secondary changes include lichenification caused by chronic scratching or weeping, maceration, and pustulation caused by bacterial superinfection.  Finally, many topical treatments may complicate the presentation by causing an allergic or irritant contact dermatitis.  DIFFERENTIAL DIAGNOSIS include psoriasis, seborrheic dermatitis, , , , familial benign , and Darier-White disease. Erythrasma fluoresces coral red under Wood lamp, unlike tinea cruris. 

 TREATMENT Most tinea cruris is successfully treated with the topical antifungals used for tinea corporis, preferably as a powder or cream. Minimizing occlusion and moisture in the area are also helpful.  As with tinea corporis, oral antifungals are reserved for refractory, widespread, or more inflammatory lesions.  Safe and effective treatment for adults includes fluconazole 150 mg weekly for 4 to 6 weeks, itraconazole 100 mg daily for 15 days, terbinafine 250 mg daily for 2 weeks, and griseofulvin 500 mg daily for 2 to 6 weeks.

Classic intertrigo secondarily infected with Candida Classic intertrigo that is probably not secondarily infected with Candida. Tinea pedis  Tinea pedis is a dermatophytosis of the feet, whereas affects the palmar and interdigital areas of the hand.  EPIDEMIOLOGY Present worldwide, tinea pedis and tinea manuum are the most common dermatophytoses.

 ETIOLOGY Tinea pedis and tinea manuum are caused predominantly by T. rubrum, T. mentagrophytes var. interdigitale, and E. floccosum.  CLINICAL MANIFESTATIONS Tinea pedis may present as any of four forms.

 Chronic intertriginous type The most common presentation of tinea pedis, the chronic intertriginous type, begins as scaling, erosion, and erythema of the interdigital and subdigital skin .  dermatophytosis simplex.  dermatophytosis complex , or “athlete's foot.

 Chronic hyperkeratotic type Usually bilateral with patchy or diffuse scaling limited to the thick skin of the feet, this is also known as “moccasin- type” tinea pedis .  T. rubrum, the most common etiology, produces very few minute vesicles, leaving collarettes of scale less than 2 mm in diameter. Erythema is variable.

 Vesiculobullous type This form, typically caused by T. mentagrophytes var. interdigitale, features tense vesicles greater than 3 mm in diameter, vesiculopustules, or bullae on the thin skin of the sole and periplantar areas.  Remissions and relapses occur with fluctuations in exposure of the feet to heat and humidity.

 Acute ulcerative type Rampant bacterial coinfection, most often from gram-negatives in combination with T. mentagrophytes var. interdigitale, produces vesiculopustules and large areas of purulent ulceration on the plantar surface. , lymphangiitis, lymphadenopathy, and fever are frequently associated.  interdigital tinea pedis without bacterial involvement can be treated topically with an allylamine, azole, ciclopirox, tolnaftate, or undecenoic acid.  The newer oral antifungals have replaced griseofulvin as the treatments of choice for severe or refractory tinea pedis. The dosing schedule of terbinafine is 250 mg daily for 2 weeks.

ONYCHOMYCOSIS

 Onychomycosis denotes any infection of the nail caused by dermatophyte fungi, nondermatophyte fungi, or . Tinea unguium, however, refers strictly to dermatophyte infection of the nail plate. The four clinical types of onychomycosis are: (1) distal subungual onychomycosis (DSO), (2) proximal subungual onychomycosis (PSO), (3) white superficial onychomycosis (WSO), and (4) candidal onychomycosis.  Onychomycosis is a common infection, with a prevalence estimated at 2 to 18 percent worldwide .  Higher rates of onychomycosis are associated with male gender, age, smoking, and peripheral arterial disease.  The dermatophytes, especially T. rubrum, T. mentagrophytes var. interdigitale, T. tonsurans, and E. floccosum, cause the great majority of onychomycosis.  DSO the most common form, begins as a whitish to brownish-yellow opacification at the distal edge of the nail or near the lateral nail fold. As the infection progresses, subungual hyperkeratosis leads to onycholysis. Increasing invasion of the ventral nail plate makes it thick, discolored, and friable. The subungual debris also provides a site for secondary infection by bacteria, other , and yeasts.

 Early PSO is evident as a white to beige opacity on the proximal nail plate that may gradually enlarge to affect the entire nail. WSO is recognized as white to dull yellow sharply bordered patches anywhere on the surface of the toenail. The affected areas are rough and friable, and may coalesce with time.

 Because onychomycosis is responsible for only 50 percent of dystrophic nails, laboratory diagnostic confirmation is often helpful prior to treatment with an oral . KOH examination, nail biopsy, and fungal culture on SDA (with and without antimicrobials) are most useful.  The only effective topical agent for tinea unguium is ciclopirox (8% lacquer) applied daily for 48 weeks .  Terbinafine is fungicidal against dermatophytes, , and Scopulariopsis, but demonstrates variable activity against Candida species.  A course of 250 mg daily for 6 weeks is effective for most fingernail infections, while a 12-week course is required for toenail infections. Most adverse effects are gastrointestinal, and cytochrome P450 interactions are insignificant.

 Itraconazole is fungistatic against dermatophytes, nondermatophyte molds, and yeasts.  Safe and effective schedules include pulse dosing at 400 mg daily for 1 week per moth.  Children may receive 5 mg/kg daily.

Erythrasma. This bacterial infection (C. minutissimum) may be confused with tinea cruris because of the similar, half-moon–shaped plaque . Erythrasma differs in that it is noninflammatory, it is uniformly brown and scaly, and it has no advancing border. The organism produces porphyrins, which fluoresce coral-red with the Wood’s light; tinea of the groin does not fluoresce.

The most common site of erythrasma is in the fourth interdigital toe space, but infection is also seen in the inframammary fold and the axillae. Erythromycin (250 mg four times a day for 5 days) or clarithromycin (single 1-gm dose) or topically to miconazole, clotrimazole, and econazole creams (but not ketoconazole).

Pitted Keratolysis , a disease mimicking tinea pedis, is an eruption of the weight-bearing surfaces of the soles. The most common sites of onset are the pressure- bearing areas, such as the ventral aspect of the toe, the ball of the foot, and the heel. Lesions are rarely seen on the non– pressure-bearing locations. Hyperhidrosis is the most frequently observed symptom. Malodor and sliminess of the skin are also distinctive features. Micrococcus sedentarius. Treatment. application of 20% aluminum chloride (Drysol) twice a day. Treatment with medications such as topical erythromycin solution or clindamycin solution is also curative. Mupirocin (Bactroban) ointment or cream and fusidic acid cream may also be effective. Oral erythromycin is an alternative.