8. Superficial Mycosis

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    SUPERFICIAL MYCOSES

    = DERMATOMYCOSES

    = SUPERFICIAL MYCOSES

    = CUTANEOUS MYCOSES

    MYCOLOGY

    Dermatophytes (literally: Skin plants)

    Separated primarily by morphology of their MACROCONIDIA and MICROCONIDIA

    Sexual forms for many Microsporum & Trichophyton spp

    Identified and assigned to genera ASCOMYCETE (Arthroderma, Nannizzia)

    Most grow best at 25 C on Sabourauds agar.

    Hyphae are spetate

    Conidia either directly on hyphae or on conidiophores

    Small microconidia may or may not be formed

    Larger & more distinct MACROCONIDIA identification

    Genus Epidermaphyton

    - Macroconidia: smooth-walled, singlt or in clusters- Micr: nil

    Genus Microsporum

    Mac: rough-walled, fusiform or culindrical

    Mic: few, pear-shaped, alone, along hyphae

    Genus Trichophyton

    Mac: smooth-walled, cylindrical

    Mic: numerous, spherical/pear shaped, appear in clusters along hyphae

    DERMATOPHYTES (Disease dermatophytosis)

    Moulds/fungi which infect KERATINIZED TISSUES (i.e superficial areas of the body) which include the

    SKIN, HAIR and NAILS

    Current number of fungal species ~ 50,000

    Those that are known to cause disease in man ~ 100-150

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    At least 40 species of dermatophytes infect humans

    Only about 15 common causes of superficial mycosis

    Classified as DEUTEROMYCETES (FUNGI IMPERFECTI)

    Family: MONOLIACEAE and 3 (THREE) GENERA

    y MICROSPORUM/ARTHRODERMA -> Infection: MICROSPOROSIS(NOT microspora! protozoa -> MICROSPORIDIOSIS)

    y Trichophyton ->INFECTION: trichophytosis(not Trichomoonas! flagellated protozoa -> TRICHOMONIASIS

    y Epidermophyton -> infection: EpidermophytosisAll the 3 fungi/GENERA have rather similar MORPHOLOGY, INFECTIVITY and PATHOGENICITY.

    Therefore usually categorized according to the CLINICAL SYNDROME and PREFERRED ANATOMIC

    SITE with which they are associated. And these superficial mycoses often manifest as serpenginous

    skin markings thereby often referred to as:

    TINEA (Latin) = grub/moth larva/worm = ringworm

    TINEA (RINGWORM) : examples

    Examples:

    Tinea Capitis Ringworm of the scalp

    Tinea Corporis Ringworm of the body

    Tinea Pedis Ringworm of the athletes foot

    Tinea Unguium Ringworm of the nails (Onychomycosis)

    Tinea Imbricata (Tokelau/Oriental ringworm) island in NZ

    Etc, etc + at least 15 others refer to big medical dictionary or dermatology textbook!

    +Tinea versicolor strictly not a dermatophytosis but included as it affects the superficial skin layers.

    EPIDEMIOLOGY

    DERMATOPHYES specially adapted to 3 sites/niches: on/in

    Humans

    Animals

    Soil Geophilic

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    y Occur worldwidey Vary in presentation according to site of infectiony High living standards

    = Lowered incidence of T. capitis

    = Increased incidence of T.Pedis (athletes foot. Shoes & stockings -> warmth & moisture)

    y Increased Dermatomycosis due to Trichophyton rubrum (an anthropophilic dermatophytethe most common dermatophyte pathogen worldwide)y Transmission of zoophilic dermatophytes

    Direct contact

    Fomites

    y Geophilic dermatophytesFarmers

    Greenhouse workers

    y The most common of the 3 anthropophilic dermatophytesPATHOGENESIS OF DERMATOPHYTOSES

    HOST FACTORS which favour disease

    Abraded skin

    Occlusive clothing, footwear, dressings

    Presence of other cutaneous diseases like atopic dermatitis

    Dermatophyte invade keratinized layer of skin -> produce keratinases that digest keratin

    Most lesions contained within this anatomic boundary

    May be self-limiting

    Widespread infection seen in patients:

    - With HIV/AIDS- On immunosuppressive drug regimes- Have endocrinopathies like Cushings disease

    Superficial Mycosis II

    Pathogenic features refer diagram

    a. Normal continual shedding of stratum corneum protects from dermatophytesb. Inflammatory reactions following dermatophytoses

    1. Penetration of stratum corneum CMI response2. Vesiculation occurs in severe cases3. Stratum corneum contains nucleated cells!

    - Inflammatory reaction increases epidermal cell division rates pass more rapidlythrough epidermis

    - Full differentiation of cells of different strate does not take place

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    4. Loss of normal translucency causing- stratum corneum to appear white- And dermal vessels to dilate

    5. Mononuclear inflammatory cells infiltrate the dermisNOTE: A crude extract called TRICHOPHYTON from certain dermatophyres produces a tuberculin-like

    response in most adults

    This contains 2 moieties ofgalactomannan

    - Carbohydrate immediate response- Peptide Delayed Type Hypersensitivity and probably immunity, too.

    CLINICAL FINDINGS

    y Superficial mycoses named according to site of infection.y These usually correspond to site of local inoculation.y Degree of inflammation often dictated by the nature of the environment from which fungus

    originates.

    y Anthrophilic dermatophytes milder IR in humansy e.g: microsporum dermii

    TINEA CAPITIS (SCALP RINGWORM)

    y Mainly affects prepubertal children ages 4-14y Often seen in- Crowded living conditions- Areas of povertyy Infection of hair shaft:y Ectothrix fungi that produces arthrospores ON hair shaft. Present with gray or

    scaling patches of alopecia with or without inflammation.y Black dot appeatance seen.y Kerions and prominent inflammatory lesion +.y Kerions = nodular, circumscribed exudative tumefaction (swelling) covered with

    pustules (usually M. canis, rarelt y T. verruocosum or T. mentagrophytes)

    y Endothrix Fungus that grows INSIDE the hair shaft.y Cuticle not destroyedy Clinically appears as simple scaling of scalp

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    y May resemble seborrheic dermatitis dandruff

    y There may be gray patches of alopecia with or without inflammation or black dotalopecia in which hair breaks off at roots

    yFavus infection leads to crusting and matter hair on the scalp with such severeinvasion that permanent alopecia often results.

    y Usually seen in Eastern Europe and Africa.TINEA BARBAE

    y Like tinea capitis, but affects the hair follicles and shafts of the facial area. Maydevelop into tumourlike abscess

    y Usual aetiologies: T. mentagrophytes, T. verrucosumTINEA CORPORIS

    y Affects non-hairy, glabrous (smooth & bare) skin.y Can be the extensions of scalp or groin infections.y Range from mild to highly inflamed lesions with pustules.y Central areas may become brown / hypoigmented and less scaly.

    TINEA CRURIS (JOCK ITCH)

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    y Commonly in men. May involve perineum, perianal and thighs.y Rarely affects srotum (cf Candida typically involves scrotum)y Typically presents with bilateral erythematous plaques with central healing. Erythematous

    border active.

    y May have vesicles and papules.y Pruritus and burning sensations most common complaints.y Infection usually transmitted from foot to groin.y Predisposing factors sweating, wet/many layered clothing

    TINEA PEDIS (ATHLETES FOOT)

    y Most common dermatophytosisy Usual cause T. rubrumy Occlusive footwear warmth and wet for fungal growthy Presents in 4 general fashions:1. Interdigital infection with erythema, maceration and scalin.2. Moccasin foot erythema and thick hyperkeratotic scales3. Inflammatory infections with vesicles, usually on the medial foot

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    4. Less common ulcerative infection affecting the web spaces of the toesy If tinea unguium (of the nails) + tinea pedis may persist due to reinfections.

    TINEA UNGUIUM (ONYCHOMYCOSIS)

    y Infection causes nails to become opaque, chalky or yellowish.y May become thickened and brittle.y Toenails more frequently unvolved.y Incidence increases with age.

    DERMATOPHYTID or ID REACTION

    y Allergic response to tinea processes that cause sterile dermatitis at distant sites.y Most common Tinea pedis itching and burning near the creases.y Vesicles and bullae may form.y Lesions may persist until primary process resolves.

    TINEA VERSICOLOR

    Aetiology:

    y Genus: Malasseziay Species: Malassezia furfur (formerly Pityrosporum orbiculare/ovale)y Organisms: Lipophilic and makes use of medium-chain length fatty acidsy Excess heat, humidity, pregnancy, oral contraceptives, malnutrition, burns and

    corticosteroids promote their proliferation.

    Clinically:

    y Begins as small circular macules of various colours (versicolor) white, pink or browndepending on hosts response reddish; hyperaemic inflammation

    yHypopigmented/hyperpigmented depends on melanosome formation in individual

    y Upper trunk most commonly affected. Highes numbers in areas of increases sebaceousactivity. Usuall asuymptomatic. Itch when inflamed.

    DERMATOPHYTOSIS DIAGNOSIS

    y Clinical manifestationsy UV (Woods) light examination in darkened roomy M. audouinii, M. canis & T. schoenleinii all give off a blue-green colour.

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    y Tinea versicolor: whitish-yellow fluorescence.y Skin/nail scrapings (keratinized/flaking material)/cutting:

    - +10-20% KOH direct microspopy hyphae- Cellophane tape Tinea versicolor.- spaghetti and meatballs appearance.

    yCulture Sabourauds agar 1-3 weeks.

    - Identified by colony colour, texturey Light microscopy morphologic patterns

    TREATMENT

    y Most tinea infections: Topical agent imidaole b.d x 2-3/52y Severe cases: oral- Itraconazole- Fluconazole- Terbinafine

    yTinea versicolor:

    - 2.5% selenium sulphide suspension (Selsun shampoo) entire body 10 minutes x 7.7- Single dose oral keto/itra/flunazole

    PREVENTION & CONTROL

    - Keep clean- Dry body surfaces all the time