s3 l23 superficial and subcutaneous mycoses

8/8/2019 S3 L23 Superficial and Subcutaneous Mycoses

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S3 L23:Superficial and Subcutaneous Mycoses by Dra.Bunyi DDD eee ccc eee mmm bbb eee rrr 111 000 ,,, 222 000 111 000

SUPERFICIAL MYCOSESInfections caused by Dermatophytes

o the so-calledkeratin-loversInfections that are superficial type

o not caused by keratin-lovers (no commondenominator)

Includes: Pityriasis (tinea) versicolor Keratomycosis Tinea Nigra Black piedra White piedra

**cannot associate one organism w/ one disease and vice versa

PITYRIASIS (TINEA) VERSICOLOR

Superficial chronic infection of stratum corneum (all of themmanifest chronically)Malassezia furfur (aka Pityrosporum orbiculare)Lyophilic yeast commensal of normal skinPathogenicity associated w/ phase change from yeast to hyphalform

o Yeast condensed milk appearance on cultureo hyphal form cottonyo Phase change affected by temperatureo Yeast form is the harmless, normal skin florao Once transformed into hyphal form, it becomes

pathogenic (Malassezia)(+) accumulation of sebum & skin oilsProliferates during times of poor hygieneTransmission:

o Skin to skin contacto Fomites

Clinical FindingsManifest early on irregular patches of hypo/hyperpigmentation w/clater coalesce to form scaly plaques

o Map-like appearance on the skino Dark colored skin hyperpigmentationo Light colored skin hypopigmentation

Noticeable on exposure to sunlightIntermittent area of scaling w/ variegated huesLight yellow & dark brown

o Shades vary from one person to another Maybe observed as infection progressesMay sometimes resolve spontaneously

o Epidemiology: many cases but they are not sobothersome to the patient that’s why they do notconsult.

(+) folliculitis in severe cases (butlig)Infection extends into hair shafts & sebaceous glandsMost commonly involved : skin of chest, back, upper armsCondition:

o Chronico irritation & inflammation absento mild pruritus

Systemic infection (parenteral lipid solution)Does not usually progress unless patient is immunocompromised

o If Malassezia had infected the skin, hardly progressesbecause of intact immune system.

DiagnosisDirect observation of skino Wood’s lamp yellow fluorescenceo Used if infection is not obviousMicroscopeo Tight clusters of spherical yeast cellso Admixed w/ hyphal fragmentso Hyphae has no septateo “spaghetti & meatballs” Cultureo Sabouraud’s Dextrose Agar o Yeast like colonies creamy consistency after 2-4 days incubation a

35oC

TreatmentTopical selenium sulfide (selenium in shampoo)

Oral ketoconazoleOral itraconazole** Must penetrate the skin to reach the fungus

KERATOMYCOSIS (MYCOTIC KERATITIS)

Posttraumatic/postsurgical corneal infectionEtiologic agents:o Saprophytic fungi

Aspergillus Fusarium Alternaria Candida)

o Histoplasma capsulatum

Clinical FindingsCorneal ulcer

DiagnosisMicroscopic finding: hyphae in corneal scrapings

TreatmentSurgery (keratoplasty)Topical pimaricinNystatin

Amphotericin B (for severe cases)

TINEA NIGRA

Exophiala werneckii produce melanin that imparts brown to blackcolor Frequent in tropical areas

Clinical FindingsBrownish maculae on palms, fingers, face, soles of feet

DiagnosisMicroscopy: septate hyphae & yeast cells (brown in color)Culture: black colonies

TreatmentTopical salicylic acidTincture of iodine

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BLACK PIEDRA

Fungal infection of the scalp hair Piedraia hortaeFrequent in tropical areas

Clinical FindingsDiscrete, hard, dark brown to black nodules on hair shafts (ectothrix – outside)

DiagnosisMicroscopy: septate pigmented hyphae and asci (sing. ascus);unicellular & fusiform ascospores w/ polar filament(s)Culture: brown to black colonies

TreatmentTopical salicylic acid Azole creams (itraconazole, miconazole)

WHITE PIEDRA

Fungal infection of scalp, facial, axillary or genital hair Trichosporon beigelii Frequent in tropical & temperate zones

Clinical findingsSoft, white to yellowish nodules loosely attached to the hair occur as asleeve or collarette around the hair shaft

DiagnosisMicroscopyo intertwined septate hyphaeo blasto- & arthroconidia (that you can find upclose)Culture: soft, creamy colonies

TreatmentShaving (but possible that spores will be left behind) Azoles

CUTANEOUS MYCOSES Tinea barbae TInea corporis Tinea capitis Tinea cruris (Jock itch) Tinea pedis (Athlete’s foot) Tinea manuum Tinea unguium

DERMATOPHYTOSIS

Tinea = ringwormInfection of the skin, hair or nails caused by a group of keratinophilicfungi called dermatophyteso Microsporum Hair, skino Epidermophyton

Skin, nailo Trichophyton

Hair, skin, nail

GENUS SPECIES

Epidermophyton E. Floccosum

Microsporum M. canisM. gypseum

Trichophyton T. mentagrophytesT. rubrumT. tonsurans

Digest kertain by their keratinasesResistant to cycloheximideClassified into 3 groups depending on their usual habitat:1. Anthrophilic

o T. rubrum2. Geophilic

o M. gypseum3. Zoophilic – affect humans & animals

o M. canis: cats & dogso M. nanum: swineo T. verrucosum: horse & swine

Pathogenesis & ImmunityContact & traumaMoisture (high in hair, groin)Crowded living conditionsCellular immunodeficiency (chronic infection)Reinfection is possible (larger inoculums needed, course is shorter)

Clinical ManifestationsInfection named according to anatomic locationo Tinea barbae bearded areao Tinea corporis bodyo Tinea capitis heado Tinea cruris groino Tinea manuum handso Tinea unguium nails

SkinCircular, dry, erythematous, scaly, itchy lesionso Redder on the outside, lighter color in the center o For microscopy, get sample in the periphery of the lesion.o Organism is not present in the center of the lesion, it is only found

border.Hair

Typical lesions, “kerion”, scarring, “alopecia” o Kerion since hair is rich in keratin

NailThickened, deformed, friableDiscolored, subungual debris accumulation

Favus (Tinea favosa ) in immunocompromised patients

TINEA BARBAE

Ringworm of the bearded areaCommon among farm workers

T. mentagrophytesLesions tend to be inflammatoryCan be spread during shavingFungal folliculitis

TINEA CORPORIS

Typicalannular lesions on the skin of the smooth parts of the body Acquired from cats & dogsSpreading, hemorrhagic border caused byT. rubrum,T.mentagrophytes, T. tonsurans T. rubrum well suited to survive on the surface of the skin chronicinfection (lifetime)



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Mannans better able to suppress CMI reactions evade hostresponse survivalSurvive off human body as spores in desquamated skin scales

TINEA CAPITIS

ringworm of the scalppeak in the early school years (M. canis)o probably due to the scissors and cloth used in the salon that is not

cleaned when used from one client to another direct contact:o infected childo variety of fomitesasymptomatic carrier statepersistenceM. audinii has been a prominent cause of children’s fungal disease Tinea capitis caused byTrichophyton tonsuransin the USGray patch ringworm communicable ectothrix infection (M.audoini/canis)Inflammatory infection (T. mentagrophytes: animal origin)Black dot ringworm endothrix infection infected degenerate hairsbreak off at the skin surface producing black dot (T. tonsurans)Fungating exophytic masses (kerions) (T. tonsurans)Favus infections T. schoenleini , T. violaceum

TINEA CRURIS (Jock Itch)

Ringworm of the groin, perineum and perianal areasE. floccossumCircinate and serpinginous w/ inflammatory vesicular, enlargingmargins May reach epidemic proportions in athletes, soldiers, ship crews Shared towels, linens, clothing More common to those who perspire freely or obese

TINEA PEDIS

Athlete’s foot most common fungal infection among adolescents (T.rubrum)

T. mentagrophytes, T. rubrum, E. flocossumMost common during warm, humid monthsOccurs in 3 main forms:1. Moccasin

o mild to severe scaling soles2. Interdigital

o peeling and cracking in the toe webs (4th web); itchy,burning or painful

3. Vesicular o sudden appearance of itchy or painful blisters (instep, heel

or ball of foot)↑keratin:soles of feet, palms of hands vulnerableCapability of T. rubrumto survive as spores in desquamated skinscales vulnerablePresent in bath towels, locker rooms, floors

TINEA UNGUIUM

Involvement of nails by dermatophyte fungiT. mentagrophytes, T. rubrum, E. flocossumOnychomycosis nail infections caused by nondermatophytic fungi( Aspergllus spp, C. albicans, Geotricum spp, etc) Begin at thelateral or distal edge of the nail plate paronychialinflammation Progresses nail becomes thickened and brittle w/ accumulation of subungual keratinized debris Nail plate separates from the nail bed split & crumble Nail may thicken, become elevated & distorted

May occur in a single nail (great toe nail) Usually lasts a lifetime, rarely healing spontaneously

TransmissionClose human contactSharing clothes, combs, brushes, towels

Animal-to-human contact

DiagnosisI. Clinical

AppearanceWood lamp (UV, 365nm)

II. Laboratory A. Direct Microscopic Examination (10-25% KOHto digest material )B. Culture

Mycobiotic agar, Saboraud’s Dextrose Agar IdentificationC. Physiologic Tests

In vitro hair perforation testSpecial amino acid and vitamin requirements

Microscopic Characteristics

MACROCONIDIUM MICROCONIDIUM

Microsporum Fusiform (+)

Epidermophyton Clavate ( - )Trichophyton (few) cylindrical/clavate/

fusiform(+) single, in clusters

Culture Characteristics

COLONY PIGMENTM. canis Cottony or wooly Lemon-yellow around

growing periphery or underside of colony

M. gypseum Sugary, granular surface

Cinnamon brown to buff

T. mentagrophytes Fluffy, granular Less intense thanT.rubrum

T. rubrum Burgundy-red

T. tonsurans flat, granular rugose w/folds radiating outwardfrom the center

Buff to tan brown

E.Flocossum suede appearance,gentle folds

Khaki or green yellow

Genus Microsporum

Macroconidiao (+) multicelled w/ thick rough wallsMicroconidiao (+) in small numberso Unevenly dispersedo Generally oval or ellipticalo No distinguishing morphologic features

1. M. canisMacroconidiao Barrel or spindle shapedo Multicelledo Pointed & slightly turned to one side at the tipo presence of spines

2. M. gypseumMacroconidiao More numerous than M. caniso Less barrel shaped w/ rounded tipso Features not always clear cut



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Genus Trichophyton Macroconidiao Typically absent or present only in small numberso Elongated & pencil shapedo Multi-celled, thin smooth wallsMicroconidiao Small, regular sizedo Abundant

1.T. mentagrophytesMicroconidiao Cluster in grapelike masses (en grappe)o Spiral hyphae may also be seen

2.T. rubrumMicroconidiao Tear shaped, regular in sizeo Distributed on either side of the hyphal strands (bird on the fence

appearance)Macroconidiao Uncommono If (+) pencil shaped thin smooth walls

3.T. tonsuransMacroconidiao NEVER seenMicroconidiao Elongated, club shaped or large balloon shaped forms admixed w/

the smaller oval or tear shaoed microconidia

Genus Epidermophyton Microconidiao ABSENTMacroconidiao Club-shaped, (+) 3-5 cellso Thin smooth wallso Cluster in groups of 3 or 4o chlamydoconidia typically present in older cultures

If microscopic morphology not distinct, perform:

UREASE HAIR BAITING TESTT. mentagrophyte Convert urea to red

color Invade shaft w/in 1-2days7-10 days conicalshaped holes

T. rubrum NegativeFaint red color after 5days

Non-invasive

Treatment Azole derivatives applied topicallyGriseofulvin: for hair infectionsFoot infections:o Acute phase: soak in KMnO4 1:5000 until acute inflammation

subsides then apply antifungalo Chronic phase:

AM – powder form PM – cream

Topicalo Miconazole, Clotrimazole, Econazole, TerbinafineOralo Griseofulvin (best because it can penetrate stratum corneum)o Ketoconazoleo Itraconazoleo Terbinafine

SUBCUTANEOUS MYCOSES

Fungi reside in soil or on vegetationTraumatic inoculation of the skin or subcutaneous tissueIn general, lesions become granulomatousLesions usually confined to the subcutaneous tissue

1. SPOROTRICHOSISSporothrix schenkii

2. CHROMOBLASTOMYCOSIS

Phialophora verrucosa Fonsecaea pedrosoi Rhinocladiella aquaspersa Fonsecaea compacta Cladosporium carrionii

3. MYCETOMA Actinomycosis

SPOROTRICHOSIS

chronic granulomatous infection with secondary spreadthe lymphaticscaused by ( Sporothrix schenkii

EpidemiologyDimorphic

Associated with grass, trees, rose bushes and other plantsGrows as a mold, have branches, septate hyphae and conidiaOccurs worldwide closely associated with plantsPredominant in malesHigher incidence in agricultural workers

Morphology and identificationGrows well on routine agar mediaYoung colonies – blackish, shiny then wrinkles with ageProduces branches, septate hyphaeand small conidia clustered at the ends

Clinical Manifestations

Conidia introduced into theskin by traumaInitial location of lesion is theextremityInitial lesion is agranulomatous nodule,eventually necroses or ulceratesLittle systemic illnessassociated inimmunocompetent hosts

Diagnosis1. Microscopic Examination of Specimen

histopathologic examination of tissue using routinefungal stain (Gomori’s or PAS)

2. Culturemost reliable method Saboraud’s agar

Treatment Oral itraconazole – treatment of choice Amphotericin B – systemic disease Other cases, self-limited



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CHROMOBLASTOMYCOSIS (CHROMOMYCOSIS)

Phialophora verrucosa Fonsecaea pedrosoi Rhinocladiella aquaspersa Fonsecaea compacta Cladosporium carrionii

EpidemiologyTraumatic inoculation of any of the 5 recognized agents thatreside in soil and vegetationProgressive granulomatous infection – hyperplasia of theepidermal tissue

MorphologySimilar in pigmentation and morphologyColonies – compact, deep brown to black, develop velvetywrinkled surfaceIdentified by their modes of conidiationProduce spherical brown cells termed as muriform or sclerotic or “Medlar” bodies

Phialophora verrucosa

Conidia from flask-shaped

phialides with cup-shapedcollarettesMature conidia accumulatearound the phialide

Fonsecaea pedrosoi

Polymorphic phialideschains of blastoconidia similar tocladosporium

Rhinociadiella aquaspersa

Produces lateral or terminalconidia from a lengtheningconidiogenous cellElliptical-shaped conidia

Cladosporium carrionii

Produce branching chains of conidia by distal budding

Clinical Findings Introduced into the skin by trauma Usual site of lesion: lower extremities (feet or legs) lesion becomes wartlike ;

cauliflower-like nodules withabscesses cover the area; “black dots” cover the wartysurface

Diagnosis

1. Microscopyo scrapings placed in 10% KOHo detection of the sclerotic

bodies is diagnostic2. Culture

o Saboraud’s agar withantibiotics

Treatmentsurgical excision : therapy of choice for small lesionsFlucytosine or itraconazole : larger lesionsRelapse - common

MYCETOMA

Actinomyces Eumycetoma

EpidemiologyChronic infection induced by traumatic inoculation with any ofsaprophytic species of fungi or actinomycetous bacteria

o Actinomycetoma – caused by actinomyceteso Eumycetoma (Madura foot)

– caused by a fungus

A. EUMYCETOMA

1. Pseudoallescheria boydii – mostcommon etiologic agent in US

2. Madurella mycetomatis – agentwhich accounts for most casesworldwide

Clinical FindingsTraumatic inoculation with soil contaminated with the agentLower extremities, hands and exposed areas are often involvedCharacterized by suppuration and abscess formationMay spread to contiguous muscles

DiagnosisIdentification of the etiologic agent is based on direct microscoexamination of the granules, culture of isolates of the agent,colonial morphology

Treatmentcombined surgical and medical treatment

o management option of choice



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*Antifungal therapy has varied results

Summary of Subcutaneous Mycoses

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Disease Agent S/Sx Identification

Sporotrichosis Sporothrix

1. Yeast2. mold

Nodules & ulcers along lymphatics& at site of inoculation

Yeast in tissue, mold at room tempwith “rosette pattern”

Chromoblastomycosis Fonsecaea Warty nodules that become“cauliflower like appearance atinoculation

Copper colored spherical yeasts called“Medlar” or sclerotic bodies in tissue

Mycetoma(Eumycetoma)

Madurella Draining sinus tracts at the site of inoculation

White, brown, yellow or black granulesin exudates that are in fungal cultures

s3 l23 superficial and subcutaneous mycoses

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