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Tinea Favosa

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Tinea Favosa Superficial Fungal Infections: Dermatophytosis The dermatophytes 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, hair, 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 . Hairs 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 Endothrix—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 bacteria, making the medium highly selective for the isolation of dermatophytes. Commercial versions of this agar are Mycosel and Mycobiotic. Dermatophyte 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, erythema nodosum, vesicular id of the hands and feet, erysipelas-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 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 folliculitis to kerion 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 lymphadenopathy, 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, atopic dermatitis, and psoriasis. Pronounced alopecia invites the consideration of alopecia areata, trichotillomania, secondary syphilis, 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 lupus erythematosus, lichen planopilaris, pseudopelade, and radiation dermatitis. TREATMENT Systemic antifungals 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 Trichophyton 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
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