PENYAKIT JAMUR KULITHIFA Vegetatif , untuk perkembangan dan pengambilan makananReproduktif, membentuk dan memperbanyak diri dengan spora

SPORASeksualAskosporaBesidosporaOosporaSigospora (debrik dari dua hifa yang sebelumnya sudah bergabung)AseksualTalosporaArtosporaBlastosporaklamidosporaKonidiosporaSporangiospora

Pembagian JamurBerdasarkan geografisTersebar luas dipermukaan bumi:TrikopitosisHistoplasmosis Hanya menyerang beberapa bagian di dunia:Blastomikosis Amerika UtaraBlastomikosis Amerika Selatan

Berdasarkan Morfologi KoloniJamur BerfilamenTrikofitonMikosporumJamur RagiKandidaJamur GandaSporotrikosis

Berdasarkan TopografiMikosis SuperfisialisDermatofitosisTinea KapitisTinea KrurisTinea KorporisTinea Pedis atau ManusTinea inguinumTinea InterdigitalisTinea FavosaTinea Barbae

Non DermatofitosisTinea VersikolorPiedra HitamPiedra Putih

b. Mikosis Intermediate: KandidasisMikosis DalamAktinomikosisNokardiasisKriptokokosisFilokomikosis SubkutisAspergilosisHistoplasmosisKromomikosisSporotrikosisBlastomikosisMisetoma (Madura Foot)

Masuknya jamur kedalam tubuhMelalui luka kecil/ aberasiMelalui saluran nafasMelalui kontak

Cara Menegakkan DiagnosaPemeriksaan preparat langsungPembiakan Reaksi ImunologisBiopsi atau pemeriksaan PAPemeriksaan dengan Sinar Wood

Kandidiasis

Definisi : Penyakit jamur yang bersifat akut atau sub akut disebabkan oleh spesies kandida biasanya oleh Candida albicans dan dapat mengenai kulit, kuku, vagina, kadang-kadang dapat menimbulkan septikemia, endokarditis, atau meningitis.

KlasifikasiKandidiasis kutan1. Intertriginosa dan perianal kandidiasis generalisata2. Paronikia dan onikomikosis3. Diaper diseases ( kandidiasis popok )4. GranulomaKandidiasis mukokutan :1. Pada mulut, thrush, glositis, stomatitis, cheilitis, perleche, vaginitis, balinitis2. Pada bronkus dan paru-paru 3. Pada saluran pencernaan, esofagus, usus dan perianal4. Kandidiasis mukokutan kronikKandidiasis sistemik

Etiologi :

Candida albicans, C. parapsilosis, C. krusei,, C. tropicalis, C. pseudotropicalis, C. lusitaniae.Genus Candida merupakan sel ragi uniseluler yang termasuk kedalam fungi imperfecti yang memperbanyak diri dengan cara bertunas.Candida hidup sebagai saprofit, merupakn flora normal pada mulut, tenggorokan, saluran cerna, vagina, lipatan kulit, ditemukan pada tanah, air, serangga dan tumbuh-tumbuhan. Jamur bimorfik, bentuk miselium atau hifa bersifat patogen, ditemukan pada penyakit sedang bentuk ragi atau klamidospor bentuk istirahat sebagai saprofit.

Gejala Klinis

Kandidiasis Kutan

Kandidiasis intertriginosaLesi berupa bercak berbatas tegas, bersisik, basah, eritematosus, dikelilingi lesi satelit berupa vesikel, pustul kecil atau bula pecah - erosif. Bentuk yang paling sering pada orang dewasa

Lokasi lesi :Lipataran kulit ketiakLipatan pahaInterglutealPerianal Lipatan payu daraAntara jari tangan atau kakiUmbilikus

Kandidiasis generalisataMengenai kulit glabrosa, bisa akibat perluasan kandidiasis intertriginosaDitemukan pada penderita dengan kondisi sistemuk yang buruk seperti DM, atau dapat juga pada orang yang berdiam lama dalam air disebut water-bath dermatitis. Lesi eritem, vesikel, pustul, mengenai daerah yang luas

Paronikia & OnikomikosisDitemukan terutama pada wanita yang sering kontak dengan air.Paronikia : jari tangan keempat dan kelima, jaringan pinggir kuku bengkak kemerahan terasa nyeri, bila ditekan keluar eksudat seperti krim.Onikomikosis: menyerang kuku, perubahan warna kuku, kuku rusak/tidak mengkilap dan menebal

Kandidiasis popokMengenai daerah perianal, perigenital, lipat paha sampai bokong.Sering pada bayi, diduga usus merupakan sumber penularanDapat pula sebagai penyebab sekunder yang menyertai penyebab primer dermatitis kontak iritan.Keluhan gatal dan perih, kulit daerah perianal eritem , edem, papul, pustul, erosif dan basah serta terdapat skuama kolaret pada tepi lesi.

Granuloma kandidaJarang ditemukan, penderitanya anak-anak, lesi mengenai wajah, kulit kepala berambut, jari tangan,badan,kaki dan faring. Lesi berupa papul hiperkeratotik yang ditutupi krusta tebal kuning kecoklatan ( granuloma)

Kandidiasis mukosa selaput lendir

A.Thrush atau stomatitis Pada bayi ( terutama ) Sakit dan panas dimulut Mulut bau asam Lesi berupa selaput ( pseudomembran) putih, coklat kelabu, bila selaput diangkat - ulkus dangkal, mudah berdarah.B.Perleche Lesi bentuk fisura pada sudut mulut, maserasi, erosi, basah, dasar eritem. Faktor predisposisi : defisiensi riboflavin.C.Vulvo vaginitis Fluor albus, mukopurulen, bau asam, perasaan gatal vagina, sering pada DM, wanita hamil.d. Balanitis Papul-papul eritem, pustul, vesikel, erosi pada glans penis & sulkus koronarius. Glans penis, sulkus koronarius dan frenulum biasanya hiperemis

Penatalaksanaan

1. Menghindari faktor predisposisi

2. Topikal Gentian violet 0,5- 2 % Nystatin Gol Azol/ non azol

3. Sistemik Nystatin Amfoterisin B Ketokonazol Flukonazol Itrakonazol

Kandidiasis intertriginosa

Kandidosis popok

Viral InfectionsDirect inoculation:V. vulgaris, M. contagiosum, Primary herpes semplex infectionSistemic infection:Varicella, AIDSLocal dispersion from internalRecurrent herpes simplex infection, Herpes Zoster

GroupSize (nm)EnvelopeNucleic acidCapsid assembly VirusDiseaseHerpes virus120-200+DNANucleusHSV tipe 1HSV tipe 2Varicella Zoster vInfeksi Herpes simplexVaricellaHerpes zosterPapova virus45-55-DNANucleusPapilloma virus humanusVerruca vulgarisCondyloma acuminataPox virus240-300-DNACytoplasmHuman pox virusMoluscum contangiosumRetro virus80-120+RNACytoplasmHIVAIDS

Skin diseases caused by virusVaricelaHerpes ZosterMoluscum ContagiosumVerrucaHerpes Simplex InfectionAIDS

VARICELLA (Chicken Pox)Defenition: Primary acute infection with Varicella Zoster Virus affected the skin and mucous membrane, clinically with constitutional symptoms, polymorph skin erruption, especially located on central part of bodyEtiology: Varicella Zoster Virus (VZV)Incidens: >> childrenIncubation Periode (IP): 14-15 days

Epidemiology:WorldwideTransmission by resp. tract and direc contactTime of transmission: a few days before I.P last to + 5 days after skin erruption

Clinical Symptoms

Prodromal Symptoms (2-3 days)Fever, malaise, cephalgia, cough+ itch

Erruption stadiumErythematous macules papules vesicles crusts (changed in 8-12 hours)Lesions of different stages are present at the same time in any given area polymorph

VesiclesThe base are surrounded by erythematous areaSuperficial (tear drops)Transparant, thin wall easily ruptured 2-3 mmFirstly serous purulent dried, start from the central (umbilication)Predilection: body, face, extremities, scalp, mucous membrane (eye, mouth, resp.tract)Distribution: central body centrifugal dispersionextremities and face

PathogenesisVZV comes inside the body via upper resp. tract multiplication disperse in blod vessel PRIMARY VIREMIAVZV was phagocytosis by RES replication in the phagocyte cells SECONDARY VIREMIAVZV disperse to the skin and mucous membrane via peripheral nerves to ganglia dorsalis (LATENT INFECTION)

DiagnosisHistory takingClinical symptomsLab examination:Tzanck smearElectron microscopeHistopathologySerologic testCulture on kidney cells of monkey

Differential DiagnosisImpetigoScabiesEczema HerpeticumDermatitis herpetiformisInsect bitePapular urticariaMolluscum Contagiosum

Complication (rare)Secondary infection by Staphylococcus & Strettococcus (impetigo, furuncle, erysipelas, cellulitis)Pneumonia children < 7 yearsMeningoencephalitisGlomerulonephritisEye complication: keratitis, vesicular conjunctivitis

The risk of complications found at:Puberty and adult patientsThe 2nd/ next patient in one familyPregnancyLow weight babyImmunocompromised patient

ManagementRestSymptomatic therapyFever antipyretics but no salicylates Reye Syndrome: - CNS disorders - hepatic disorders - cerebral oedemaItch antihistamineSecondary infection antibiotics

TopicalSalicyl talc 2% unruptured vesiclesAntibiotics zalf ruptured vesicles/ crustsWet dressings with Burrows solution

Antivirus Efective < 24 hours erruption (+)Acyclovir: infant/child: 4x20 mg/BB weight (5-7 days) adult: 5x800 mg/day (5-7 days)Valacyclovir: 3x1000 mg/day (7day)Famcyclovir: 3x250 mg/day

PrognosisImmunocompetent patient goodImmunocompromised worsePregnant women, 1st trimester Congenital Varicella Syndrom (cutaneous scars, CNS abnormality, atrophy of the eye, limb hypoplasia)Neonatal varicella:Transmitted frm pregnant women who suffering from varicela 5 days before deliverySevere symptoms

PreventiveIsolationVaccination:To prevent complicationIf suffering mild symptomsVaricela Zoster Immunoglobulin (VZIG)Pregnant womanNeonate mother (+) varicellaIM 4 days after exposure

HERPES ZOSTER (ZOSTER=SHINGLES)

Definition: Skin disease caused by Varicella Zoster Virus, involving the skin of single/several dermatome, as the viral reactivation after primary infection

PathogenesisVZV dorman at the posterior ganglion of the periphery nervous system and cranial ganglion reactivation via the axon travelled to the skin replication & multiplication characteristics lesion on dermatomeSometimes affected the anterior ganglion, motoric cranialis part motoric disorders symptoms

EpidemiologyAffected the person who have been infected with varicella beforeViral reactivation may caused by CMI , local trauma, radiotherapy, malignancy, HIV infection, etcUsually adult, man=woman

Clinical ManifestationsProdromal phase (1-2 days)Constitusional symptoms: fever, headache, malaiseLocal symptoms: pain, burning, itchyErruptional phase groups of vesicles on erythematous base, situated unilaterally, of dermatomeMostly: thoracal, lumbosacral, cervical, facial

Variant HZHZ ophtalmicus N.V ramus ophtalmicusSyndrom Ramsay Hunt N VII, N VIIIHZ DisseminataSacral ZosterHZ aberansZoster sine herpetteHZ Bilateral

ComplicationsNeuralgia post HZGangren superficialisSecondary infectionsEye complicationsHZ disseminata/ generalisataSistemic complications

ManagementTopical applicationSalicyl talc 2 % prevent the vesicles to ruptureWet dressings with antiseptic solution ruptured vesicles/& wet lesionsAntibiotic zalf crusts

II. Sistemic therapyPatient without immunologic disordersAge

Age >50 yearsSevere symptomsSimptomatic therapyAcyclovir 5x800 mg/day (7-10 days) orValacyclovir/ FamcyclovirWidespread lesion: Acyclovir i. 3x10 mg/kg BW/days (5 days)

B. Patient with immunologic disordersAll agesAcyclovir 7,5-10 mg/kg BW every 8 hours (7 days)AIDS patientFrequently resistanceFoscarnet i.v 60 mg/kg BW every 8 hours (14-21 days)HZ ophtalmicusAcyclovir: 10 daysHZ on pregnancyNo Acyclovir except HZ ophtalmicus/ Sindrom Ramsay Hunt

MOLLUSCUM CONTAGIOSUMDefinition:skin disease caused by Human Pox Virus umbilicated papule discrete or in a groupI.P: 1-8 weeksIncidence: >>childrenEpidemiology: WorldwideGenital lesion sex intercourse

PathogenesisVirus evolve in the cytoplasm of epidermal cells (str. Malphigi & str. Granulosum) infected cells growth fastly (proliferation) to the upper of epidermis.Clinically: papules contain of debris cells, virus, and fibrotic tissue Molluscum bodies (white colored, rice-looked mass)

Clinical ManifestasionsSmall flesh/ whitish papule, waxy, dome shaped, which are umbilicated (delle) 3-6 mm, in some case Giant MolluscumPredilection: face, chest, arm, genital, mucous membrane (lip, tongue, buccal)Lesions are spread by autoinoculation and skin contact transmission

DiagnosisClinical manifestationCytology: infected cells can be examined directly in heated potassium hydroxyde preparationHistopathology: Molluscum bodies which contain viral particles was found at the epidermis

DDVerrucaVaricellaFuruncleLichen planusMilliumKeratoacanthoma

ManagementPrinciples: to exclude the molluscum bodies contained-massTreatment:CurretageThe lessions is scraped away with a curette then topical antibiotics may put onCryosurgeryElectrocautery

VERRUCA (WARTS)DefinitionSkin disease caused by Human Papilloma Virus (HPV) infection, which is a benign-verrucous vegetation or papillomaEtiologyHPV, which have several distinct typeType 16, 18, 31, 33, 35 malignancy

EpidemiologyWorldwideTransmission via skin contact and autoinoculationDepends on the type of the warts, some appear at children while others at adult

PathogenesisViral warts are tumors initiated by a viral infection of keratinocytes the cell proliferate and form mass hard verrucous papilloma

ClassificationClinical variant:Verruca vulgarisVerruca plana juvenilisVerruca plantarisCondyloma accuminata

1. VERRUCA VULGARIS (common wart)Rounded papul, grayish, verrucous surfaceKoebner Phenomena (+)Predilection: extensor extrimity, dorsum manus and pedis, fingers and toesSometimes self-limitedChiefly in children

VERRUCA PLANA JUVENILIS (flat wart)rounded/ polygonal, smooth, flat-surfaced lesion, 1-5 mm, flesh coloured or brownishPredilection: face,neck, dorsum manus and pedis, wrist and kneeKoebner Phenomena (+)Chiefly in children and juvenileVERRUCA PLANTARISSoft, pulpy cones and surrounded by a firm horny ring on the sole

DDTBC Cutis VerrucosaKeratoacanthomaLichen planusClavusKeratoderma punctata

ManagementKeratolytic agent: salicylic acid 40% (10-14 days) curettageCryosurgery: CO2, liquid NitrogenElectrocauteryExcision

HERPES SIMPLEX INFECTION (HS)Def: chronic infection caused by Herpes Simplex Virus (HSV), characteristics with group of vesicles on erythematous base, involving the skin and mucous membrane, maybe primary or recurrent

VHS 2 type:VHS type I: mostly HS labialis (orofasial)VHS type II: mostly HS genitalis

EpidemiologyWorldwideTransmission by direct contactMay be transmitted to the baby: prenatal, delivery, post natal

PathogenesisVirus comes inside the body via the lip, mouth, skin, conjunctiva, genital, nostrils multiplication reg. lymph node and blood vessels skin and mucous membrane replication primary lesion (group of vesicles) viral travelled to ganglion radix dorsalis following the peripheral nerves sheet viral dorman (latent period) reactivation recurrent lesions

Clinical ManifestasionsItchy/ burning/ reddish few minutes hours vesicles (+)Serous vesicles seropurulent ruptured in a few days crusts healed in 1 week without scarring(+) lymph nodePredilection: lip, genital

VariantHerpes labialisHerpes genitalisHerpetic WhitlowEksema herpetiformisHS OcularHS Encephalitis

DiagnosisHistory takingClinical ManifestationsTzanck testKulturSerology: Ab Specific HSV I & HSV II

DDBullous impetigoStomatitis aphtosaOral thrush

ManagementSimptomatic analgeticsAntiviral:Acyclovir 5x200 mg (7 days)Valacyclovir 2x500 mg (7 days)Famcyclovir 3x250 mg (7 days)Severe complication: intravenous Acyclovir

SuggestionIf lesions (+) abtinentia sexual/ condomsHealth educationExaminations of sexual partner

MelasmaLentigenosisEfelidLentigo SenilisMelanosis RiehlPenebalan warna karena logamArgiriaBismutEmas

Perubahan warna kulit karena obatMinosiklinKlorpromazinKlofaziminKaroten

HemokromatosisKarotenosisLikopeniaVitiligoAlbinisme okulokutaneusSindrom AlejandreniSindrom Chediak HigashiPielbaldismLeukoderma

Melasma

Berupa makula coklat muda coklat tuaMengenai daerah yang terpajan sinar UV yaitu pipi, dahi, daerah atas bibir, hidung dan daguDi Indonesia perbandingan wanita : pria 24:1

Faktor KausatifSinar UVHormon (estrogen, progesteron, dan MSH)Obat (minosiklin, klorpromazin)Genetik (20%-90%)Ras (kulit berwarna gelap)Kosmetika (parfum, zat pewarna)Idiopatik

KlasifikasiSentrofasial (63%)Malar (21%)Mandibular (16%)

Pemeriksaan dengan Sinar WoodTipe epidermallesi lebih kontrasTipe dermallesi tidak bertambah kontrasTipe campuranTipe tidak jelas

PencegahanPemakaian tabir matahariMenghilangkan faktor penyebabPengobatanTopikalHidrokuinon 2-5%Asam retinoat 0,1%Asam azeleat 20%6 blnSistemikAsam askorbat

Tindakan KhususPengelupasan kimiawiBedah laser

LentiginosisMakula coklatcoklat kehitamanEtiologi: bertamabahnya jumlah melanositpada taut dermo epidermal

EfelidMakula hiperpigmentasi coklat terang pada kulit yang sering terkena UVSinonim: FrecklesLebih sering terjadi pada orang kulit putih

Melanosis RiehlDermatitis akibat fotosensitivitasPruritus, eritem, pigmentasiEtiologi belumdiketahui pastiPenyebab: nutrisi, derivat ter, bahan pewangi dan kosmetika

Perubahan warna karena logamArgiriaBerupa pigmen keabuan pada daerah yang terkena sinar UV (muka, tangan, mukosa mulut, dan sklera).BismuthKalau dimakan, pewarnaan pada gusi, stomatitis.EmasPigmentasi warna abu-abu atau nila pada kelopak mata.MerkuriWarna coklat abu-abu pada muka dan leher

LikopeniaPigmen merah pada tomat , bit dan cabe.

VitiligoDefenisiVitilgo adalah hipomelanosis idiopatik dengan makula putih yang dapat meluas.

EpidemiologiInsidensi 0,1-8,8 %. Awitan terbanyak sebelum umur 20 tahun. Pada penderita vitiligo 5%akan mempunyai anak dengan vitiligo.Riwayat keluarga 20-40%

Faktor PencetusKrisis emosiTrauma fisis

KlasifikasiLokalisasiFokalSegmentalmukosal

GeneralisataAkrofasialVulgariscampuran

TerapiPsoralen 0,6 mg/kgBB6 bln1 thnUsia18 thngeneralisatasistemik kapsulMetoksalen 20 mg2jamjemur, 3x/minggu6 bln