REFERAT
MORBUS HANSEN
Disusun oleh : Sitti Monica Astrilia Ambon (030.09.239)
Pembimbing : dr. Dewi Anggreni, Sp.KK dr. Iwan Trihapsoro, Sp.KK, Sp.KP, FINSDV, FAADV dr. A.A. Sri Budhyani
KEPANITERAAN KLINIK ILMU KULIT DAN KELAMIN RSAU DR.ESNAWAN ANTARIKSA UNIVERSITAS TRISAKTI PERIODE 2 JUNI 2014 – 5 JULI 2014, JAKARTA
0
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MORBUS HANSEN
I.
PENDAHULUAN Morbus Hansen yang disebut juga Lepra adalah infeksi kronik yang disebabkan oleh Mycobacterium leprae, leprae, yang merupakan mikroorganisme yang menyerang kulit dan saraf. Meskipun tidak fatal, lepra merupakan salah satu penyebab paling sering neuropati perifer di seluruh dunia. Penyakit ini telah ada di dunia sejak lama. DNA yang diambil dari mayat di kota Jerusalem menunjukkan bahwa Ia merupakan manusia pertama yang menderita lepra. Penyakit ini kemungkinan berasal dari Mesir dan Negara Timur Tengah lainnya pada awal 2400 SM. Kurangnya pengetahuan di masa itu mengenai penyakit tersebut menyebabkan penyakit tersebut menyebar ke seluruh penjuru dunia.
Mycobacterium leprae,
penyebab dari lepra
ditemukan oleh G.H Armauer Hansen di Norway pada tahun 1873. Lebih dari 20 tahun , imlementasi WHO terhadap kasus MDT (Multi Drugs Resistance) telah membuat prevalensi infeksi lepra menurun sekitar 90 % di Negara endemic dengan kurang dari satu kasus dalam 10.000 populasi. Walaupun, pada Negara-negara seperti Brazil, Congo, Madagascar, Mozambique, Nepal, dan Tanzania.1,11
II.
EPIDEMIOLOGI Kusta terdapat dimana-mana, terutama di Asia, Afrika, Amerika latin, daerah tropis dan subtropis, serta masyarakat yang sosial ekonominya rendah. Makin rendah sosial ekonomi rendah makin berat penyakitnya, sebaliknya faktor sosial ekonomi tinggi sangat membantu penyembuhan. Pada tahun 1991 World Heath Assembly membuat resolusi tentang eliminasi kusta sebagai problem kesehatan masyarakat pada tahun 2000 dengan menurunkan prevalensi kusta menjadi dibawah 1 kasus per 10.000 penduduk. Di indonesia dikenal dengan Eliminasi Kusta tahun 2000 (EKT 2000). 2 Peyakit ini masih teteap menjadi endemik di Negara seperti Afrika dan
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terdeteksi 85 % kasusnya dalah kasus baru. Contohnya pada tahun 2009 di India terdapat 94 % kasus lepra baru dari 79 % populasi saat itu. Pada tahun 2005 – – 2007 di Brasil 17 % dari populasi berkontribusi pada 53 % kasus baru. Untuk Indonesia sendiri pada tahun 2007, 14 dari 33 provinsi terdapat 83 % kasus baru. Sedangkan China pada tahun 2009, 3 dari 31 provinsi mempunyai 54, 5 % kasus baru.
III.
3
ETIOLOGI Mycobacterium leprae belum berhasil dibiakan secara secara in vitro. Mycobacterium leprae berkembang biak pada suhu 30 - 33°C dalam waktu 12 hari. Mikroorganisme ini merupakan mikroorganisme yang kuat yang dapat bertahan hidup di lingkungan selama 10 hari. 4 Kuman ini ditemukan oleh G.A Hansen pada tahun 1874 di Norwegia. M. leprae merupakan kuman Gram positif yang berbentuk basil dengan ukuran 3 – 3 – 8 8 Um x 0,5 Um, yang mempunyai komponen antigenik kompleks yang terdiri dari lipid, karohidrat dan protein, sehingga kuman ini tahan asam dan alkohol.2,4
IV.
PATOGENESIS Faktor risiko untuk terjadinya lepra adalah lahir atau tinggal di area yang diketahui sebagai daerah endemic, ada keluarga yang menderita lepra, mempunyai genetic, terpapar dari lingkungan sekitar, dan kemiskinan. Meskipun cara masuk M. leprae leprae ke dalam tubuh masih belum diketahui dengan pasti, beberapa penelitian telah memperlihatkan bahwa yang tersering adalah melalui kulit yang lecet pada bagian tubuh yang bersuhu dingin dan melalui mukosa nasal. Pengaruh M. leprae leprae terhadap kulit bergantung pada faktor imunitas seseorang. Oleh karena itu penyakit kusta dapat disebut sebagai penyakit imunologik. Gejala klinisnya sebanding dengan tingkat reaksi selularnya daripada intensitas infeksinya.4,13 Sebagai proteksi awal sebelum bakteri masuk ke dalam kulit, terutama kompartemen imunologik bakteri tersebut harus melewati beberapa sawar, salah satunya adalah berbagai mekanisme non-spesifik seperti sistem
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mengeliminasi bakteri, sehingga pada 95% individu yang terinfeksi oleh M. leprae leprae tidak menimbulkan gejala klinis atau minimal hanya subklinis saja. Setelah berbagai sawar nonspesifik tersebut gagal, maka barulah akan bekerja
mekanisme
imunitas
spesifik,
melalui
aktivasi
sel-sel
imunokompeten oleh stimulasi antigen M. leprae. leprae.5 Bila basil M. leprae leprae masuk ke dalan tubuh seseorang, dapat timbul gejala klinis sesuai dengan kerentanan orang tersebut. Bentuk tipe klinis bergantung kepada sistem imunitas seluler (SIS) penderita. SIS yang baik akan tampak gambaran klinis kearah tuberkuloid, sebaliknya SIS rendah memberikan gambaran lepromatosa. Makrofag dalam jaringan yang berasal dari monosit di dalam darah ada yang mempunyai nama lain sel Kupffer di hati, sel alveolar di paru, sel glia dari otak, dan yang dari kulit disebut histiosit. Salah satu tugas makrofag adalah melakukan fagositosis. Kalau ada kuman masuk, akibatnya akan bergantung pada SIS. Apabila SIS-nya tinggi, makrofag akan mampu memfagosit M. leprae. leprae. Datangnya histiosit ke tempat kuman disebabkan karena proses imunologik dengan adanya faktor kemotaktik. Kalau datangnya berlebihan dan tidak ada lagi yang harus difagosit, makrofag akan berubah bentuk menjadi sel epiteloid yang berlebihan dikelilingi oleh limfosit yang disebut tuberkel. Apabila SIS rendah atau lumpuh, histiosit tidak dapat menghancurkan M. leprae yang leprae yang sudah ada di dalamanya, bahkan dijadikan tempat berkembang biak dan disebut sel Virchow atau sel lepra atau sel busa dan sebagi alat pengangkut penyebarluasan.5,6 Pada kusta tipe LL terjadi kelumpuhan sistem imunitas selular, dengan demikian makrofag tidak mampu menghancurkan kuman sehingga kuman dapat bermultiplikasi dengan bebas yang kemudian dapat merusak jaringan. Kelainan kulit yang terjadi lebih ekstensif. Lesi kulit terdiri dari nodus yang infiltratis dan plak. Kelainan saraf dapat simetris. 5,6,7
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Gambar 1. Imunitas terhadap bakteri Sumber : Playfair JHL, Chain BM. Immunity to bacteria. Immunology at a Glance
Pada kusta tipe TT kemampuan fungsi sistem imunitas selular tinggi, sehingga makrofag sanggup menghancurkan kuman. Sayangnya setelah semua kuman difagositosis, makrofag akan berubah menjadi sel epiteloid yang tidak bergerak aktif dan kadang-kadang bersatu membentuk sel datia Langhans. Bila infeksi ini tidak segera diatasi akan terjadi reaksi berlebahan dan masa epiteloid akan menimbulkan kerusakan saraf dan jaringan sekitarnya. Tipe ini biasanya menyerang kulit dan saraf perifer. Jumlah lesi kulit terbatas dengan kulit kering dan hipoanestesia. Kelainan saraf biasanya asimetris. 7 Sel Schwann merupakan sel target untuk pertumbuhan M. leprae sehingga menyebabkan cedera pada saraf, demielinasi, dan akibatnya, cacat. Pengikatan M. leprae ke sel Schwann menyebabkan demielinisasi
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setelah itu mengaktifkan CD4+. CD4+ akan mengaktifkan Th1 dan Th2 dimana Th1 dan Th2 akan mengaktifkan makrofag. Makrofag gagal memakan M. leprae akibat adanya fenolat glikolipid I yang melindunginya di dalam makrofag. Ketidakmampuan makrofag akan merangsang dia bekerja terus menerus untuk menghasilkan sitokin dan GF yang lebih banyak lagi. Sitokin dan GF tidak mengenai bagian self atau nonself sehingga akan merusak saraf dan saraf yag rusak akan diganti dengan jaringan fibrous sehingga terjadilah penebalan saraf tepi.7 V.
GAMBARAN KLINIS Sebelum
membahas
mengenai
gambaran
klinis
akan
dibahas
mengenai klasifikasi terlebih dahulu. Ridley dan Jopling memperkenalkan istilah spectrum determinate pada penyakit lepra yang terdiri atas berbagai tipe, yaitu: IL
: Indeterminate leprosy
TT
: Tuberkuloid polar, bentuk yang stabil
BT
: Borderline tuberculoid
BB
: Mid borderline
BL
: Borderline lepromatous
LLs
: Lepromatous subpolar
LLp
: lepromatosa polar, bentuk yang stabil
bentuk yang labil
TT adalah tipe tuberkuloid polar, yakni tuberkuloid 100%, tipe yang stabil. Jadi tidak mungkin berubah tipe. Begitu juga LLp adalah tipe lepromatosa polar, yakni lepromatosa 100%. Sedangkan tipe antara BT dan LLs disebut tipe borderline atau campuran, berarti campuran antara tuberkuloid dan lepromatosa. BB adalah tipe campuran 50% tuberkuloid dan 50% lepromatosa. BT lebih banyak tuberkuloidnya, sedang BL dan LLs lebih banyak lepromatosanya. Tipe-tipe campuran ini adalah tipe yang labil, berarti dapat beralih tipe, baik ke arah TT maupun LLp. 7 Indeterminate leprosy tidak termasuk dalam spektrum.2
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Tabel 1. Klasifikasi Ridley-Jopling Sumber : Ridley DS, Jopling WH. Classification of leprosy according to immunity: a five-group system. I nt J Leprosy 1966; 54 : 255-73
Menurut WHO (1981), lepra dibagi menjadi multibasilar (MB) dan pausibasilar (PB). Multibasilar berarti mengandung banyak basil dengan indeks biposi (IB), ditemukan bakteri lebih dari +2, yaitu tipe LLp, BL, dan BB pada klasifikasi Ridley-Joping. Pausibasilar mengandung sedikit basil dengan IB kurang dari +2, yaitu tipe TT, BT, dan I klasifikasi Ridley-Joping.2
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Zona spectrum kusta menurut berbagai klasifikasi dapat dilihat dibawah:2 Klasifikasi Ridley&Jopling Madrid
Zona spectrum kusta TT
BT
Tuberkuloid
BB
BL
Borderline
LL Lepromatosa
WHO
Pausibasilar (PB)
Multibasilar (MB)
Puskesmas
PB
MB
Masa inkubasinya 2 – – 40 tahun (rata-rata 5 – – 7 tahun). Onset terjadinya perlahan-lahan dan tidak ada rasa nyeri. Pertama kali mengenai sistem saraf perifer dengan parestesi dan baal yang persisten atau rekuren tanpa terlihat adanya gejala klinis. Pada stadium ini mungkin terdapat erupsi kulit berupa macula dan bula yang bersifat sementara. Keterlibatan sistem saraf menyebabkan kelemahan otot, atrofi otot, nyeri neuritik yang berat, dan kontraktur tangan dan kaki. Gejala prodromal yang dapat timbul kadang tidak dikenali sampai lesi erupsi ke kutan terjadi. 90% pasien biasanya mengalami keluhan pada pertama kalinya adalah rasa baal, hilangnya sensori suhu sehingga tidak dapat membedakan panas dengan dingin. Selanjutnya, sensasi raba dan nyeri, terutama dialami pada tangan dan kaki, sehingga dapat terjadi komplikasi ulkus atau terbakar pada ekstremitas yang baal tersebut. Bagian tubuh lain yang dapat terkena kusta adalah daerah yang dingin, yaitu daerah mata, testis, dagu, cuping hidung, daun telinga, dan lutut.2 Perubahan saraf tepi yang terjadi dapat berupa (1) Pembesaran saraf tepi yang asimetris pada daun telinga, ulnar, tibia posterior, radial kutaneus, (2) Kerusakan sensorik pada lesi kulit (3) Kelumpuhan nervus trunkus tanpa
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tidak ada. Karakteristik khas yang biasa didapatkan pada biopsi kulit lepra tidak didapatkan pada IL. 9 Biasanya muncul pada wajah, bagian ekstensor dari ekstremitas, pantat atau dada.
Gambar 2. Indeterminate Leprosy Sumber : Lockwood DNJ. Leprosy. Rook’s Textbook of Dermatology
2. Tuberculoid Leprosy (TT) TT merupakan bentuk lepra yang paling ringan. Imunitas host biasanya masih baik, dapat sembuh spontan dan masih mampu melokalisir sehingga didapatkan gambaran batas yang tegas. Mengenai kulit maupun saraf. Lesi kulit bisa satu atau beberapa, dapat berupa makula atau plak, dan pada bagian tengah dapat
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hipopigmentasi, kekeringan kulit atau skuama tidak sejelas TT. Gangguan saraf tidak berat dan asimetris. 9
Gambar 3. Tuberculoid Leprosy Sumber : Lockwood DNJ. Leprosy. Rook’s Textbook of Dermatology
3. Lepromatous Leprosy (LL) Manifestasi klinis awal yang muncul biasanya di kulit (karena gejala saraf biasanya masih asimptomatik pada awal penyakit), namun biasanya tidak terlalu diperhatikan oleh pasien, mereka lebih sering mengeluhkan keluhan seperti keluhan hidung tersumbat disertai adanya sekret dan epistaksis. Untuk daerah kulit sendiri jumlah lesi sangat banyak, nodul mencapai ukuran 2 cm, simetris, permukaan halus, lebih eritematous, berkilap, berbatas tidak tegas dan pada
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progresif
membentuk
facies
leonine.
Kerusakan
menyebabkan gejalan stocking and glove anesthesia. anesthesia .9
Gambar 4. Lepromatous Leprosy Sumber : Lockwood DNJ. Leprosy. Rook’s Textbook of Dermatology
saraf
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Gambar 6. Hidung pelana dan infiltrasi pada lidah Sumber : Lockwood DNJ. Leprosy. Rook’s Textbook of Dermatology
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Gambar 8. Multiple dermatofibroma-like pada LL Sumber : Lee DJ, Rea TH, Modlin RL. Leprosy. Fitzpatrick’s Dermatology in General Medicine
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waktu dapat mengalami down-grades menjadi LL (apalagi bila tidak diobati), atau mengalami upgrades menjadi TT.4
Gambar 9. Borderline Tuberculoid (BT) Sumber : Lockwood DNJ. Leprosy. Rook’s Textbook of Dermatology
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Gambar 11. Borderline (BB) Sumber : Lockwood DNJ. Leprosy. Rook’s Textbook of Dermatology
Deformitas dapat terjadi pada kusta. Pada kusta sesuai dengan
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tak mampu ekstensi jari-jari atau pergelangan tangan. Pada N. Poplitea lateralis adalah anestesi tungkai bawah, bagian lateral, dan dorsum pedis, kaki gantung (foot (foot drop) dan kelemahan otot peroneus. Pada N. Tibialis posterior adalah anestesi telapak kaki, claw toes dan paralisis otot intrinsik kaki dan kolaps arkus pedis. Pada N. Fasialis adalah cabang temporal dan zigomatik menyebabkan lagoftallmus dan cabang bukal, mandibular serta servikal
menyebabkan
kehilangan
ekspresi
wajah
dan
kegagalan
mengatupkan bibir. Pada N. Trigeminus adalah anestesi kulit wajah, kornea dan konjungtiva mata. Kerusakan mata pada kusta dapat primer dan sekunder. Primer mengakibatkan alopesia pada alis mata dan bulu mata (madarosis), juga dapat mendesak jaringan mata lainnya. Sekunder disebabkan oleh rusaknya N. Fasialis yang menyebabkan paralisis orbikularis okuli sebagian atau seluruhnya, mengakibatkan lagoftalmus yang selanjutnya menyebabkan kerusakan bagian-bagian mat alainnya. Secara sendirian atau bersama-sama menyebabkan kebutaan. Infiltrasi granuloma ke dalam adneksa kulit yang teriri atas jaringan keringat, kelenjar palit, dan folikel rambut dapat menyebabkan kulit kering dan alopesia. Pada tipe lepromatous dapat timbul ginekomastia akibat ganggguan keseimbangan hormonal dan oleh karena infiltasi granuloma pada tubulus semineferus
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yang memadai. Tipe lepra yang termasuk borderline ini dapat bergerak bebas ke arah TT dan LL dengan mengikuti naik turunnya SIS, sebab setiap perubahan tipe selalu disertai perubahan SIS pula. Begitu pula reaksi reversal, terjadi perpindahan tipe ke arah TT dengan disertai peningkatan SIS, hanya bedanya dengan cara mendadak dan cepat. Gejala klinis reaksi reversal ialah umumnya sebagian atau seluruh lesi yang telah ada bertambah aktif atau timbul lesi baru dalam waktu relatif singkat. Artinya lesi hipopigmentasi menjadi eritema, lesi eritema menjadi lebih eritematosa, lesi makula menjadi infiltrat, lesi infiltrat menjadi makin infiltratif dan lesi lama menjadi bertambah luas. Adanya gejala neuritis akut penting diperhatikan, karena sangat menentukan pemberian pengobatan kortikosteroid. 4,10,12
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Eritema nodosum leprosum (E.N.L.) / type 2 ENL timbul terutama pada tipe LL dan BL. Secara imunopatologis, ENL termasuk respons imun humoral, berupa fenomena kompleks imun akibat reaksi antara antigen M. leprae leprae + antibodi (IgM, IgG) + komplemen
kompleks imun. Hal ini terjadi karena pada tipe lepromatosa jumlah basil jauh lebih banyak daripada tipe tuberkuloid. ENL lebih banyak terjadi pada tahun kedua pengobatan karena banyak basil lepra yang mati dan hancur, berarti banyak antigen yang dilepaskan dan bereaksi dengan antibodi, mengaktifkan sistem komplemen. Kompleks imun tersebut terus beredar dalam sirkulasi darah yang akhirnya dapat melibatkan berbagai organ. 2,12 Pada kulit akan timbul gejala klinis yang berupa nodus eritema dan nyeri dengan tempat predileksi di lengan dan tungkai. Bila mengenai organ lain dapat menyebabkan gejala seperti iridosiklitis, neuritis akut, limfadenitis,
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Fenomena Lucio Fenomena Lucio merupakan reaksi kusta yang sangat berat yang terjadi pada kusta tipe lepromatosa non-nodular difus. Kusta tipe ini terutama ditemukan di Meksiko dan Amerika Tengah, namun dapat juga dijumpai di negeri lain dengan prevalensi rendah. Gambaran klinis dapat berupa plak atau infiltrate difus, berwarna merah muda, bentuk tak teratur dan terasa nyeri. Lesi terutama di ekstremitas, kemudian meluas ke seluruh tubuh. Lesi yang berat tampak lebih eritematosa, disertai purpura, dan bula kemudian dengan cepat terjadi nekrosis serta ulserasi yang nyeri. Lesi lambat menyembuh dan akhirnya terbentuk jaringan parut. 2 Gambaran histopatologi menunjukkan nekrosis epidermal iskemik dengan nekrosis pembuluh darah superfisial, edema, dan proliferasi endothelial pembuluh darah lebih dalam. Didapatkan banyak basil M. leprae
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VI.
PEMERIKSAAN PENUNJANG 1. Pemeriksaan Bakterioskopik Sediaan dari kerokan jaringan kulit atau usapan mukosa hidung yang diwarnai dengan pewarnaan BTA ZIEHL NEELSEN. Pertama – tama – tama harus ditentukan lesi di kulit yang diharapkan paling padat oleh basil setelah terlebih dahulu menentukan jumlah tepat yang diambil. Untuk riset dapat diperiksa 10 tempat dan untuk rutin sebaiknya minimal 4 – 6 – 6 tempat yaitu kedua cuping telinga bagian bawah dan 2 -4 lesi lain yang paling aktif berarti yang paling eritematosa dan paling infiltratif. Pemilihan cuping telinga tanpa menghiraukan ada atau tidaknya lesi di tempat tersebut karena pada cuping telinga biasanya didapati banyak M. leprae.2 Kepadatan BTA tanpa membedakan solid dan nonsolid pada
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dan non solid. Tipe lepromatosa terdapat kelim sunyi subepidermal ( subepidermal clear zone ) yaitu suatu daerah langsung di bawah epidermis yang jaringannya tidak patologik. Bisa dijumpai sel virchow dengan banyak basil. Pada tipe borderline terdapat campuran unsur – unsur – unsur unsur tersebut. Sel virchow adalah histiosit yang dijadikan M. leprae leprae sebagai tempat berkembangbiak dan sebagai alat pengangkut penyebarluasan. 2 3. Pemeriksaan Serologik Didasarkan terbentuk antibodi pada tubuh seseorang yang terinfeksi oleh M.leprae. Pemeriksaan serologik adalah MLPA (Mycobacterium Leprae Particle Aglutination), Aglutination), uji ELISA dan ML dipstick, PCR. 2 4. Tes Lepromin
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1.
Bercak kulit yang mati rasa Pemeriksaan harus di seluruh tubuh untuk menemukan lesi di bagian
tubuh
yang
hipopigmentasi
atau
lain,
biasanya
eritematous,
lesi
mendatar
dengan
bercak
(makula)
atau
meninggi (plak). Mati rasa pada bercak bersifat total atau sebagian saja terhadap rasa raba, rasa suhu dan rasa nyeri. 8 2.
Penebalan saraf tepi
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Pityriasis versikolor Pada pityriasis versikolor tidak selalu bersisik, dan daerah distribusinya pada punggung dan dada serta gambaran makulanya berbeda dengan pada lepra.
Tinea Korporis Pada tinea korporis lesi dirasakan sangan gatal dan bisa terdapat vesikel pada pinggirannya dan pada kerok kulit didapatkan jamur.
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Lamprene atau Clofazimin, merupakan bakteriostatik dan dapat menekan reaksi kusta. Clofazimin bekerja dengan menghambat siklus sel dan transpor dari NA/K ATPase. Efek sampingnya adalah warna kulit bisa menjadi berwarna ungu kehitaman,warna kulit akan kembali normal bila obat tersebut dihentikan, diare, nyeri lambung.3 Rifampicin, bakteriosid yaitu membunuh kuman. Rifampicin bekerja dengan cara menghambat DNA-dependent RNA polymerase pada sel
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Tabel 2. Regimen pengobatan kusta dengan lesi tunggal (ROM) menurut WHO/DEPKES RI
Dewasa (50-70 kg)
Rifampicin
Ofloxacin
Minocyclin
600 mg
400 mg
100 mg
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Tabel 4. Regimen MDT pada kusta Multibasiler (MB) Rifampicin Dewasa
600
mg/bulan 100
Dapson
Lamprene
mg/hari 300 mg/bulan diminum
diminum di depan diminum di rumah
di
depan
petugas
petugas
kesehatan
kesehatan
dgn 50 mg/hari diminum
dilanjutkan
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levofloksasin dengan dosis 500 mg sehari. Obat tersebut lebih baru,
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b. Penderita yang menolak klofazimin
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pada berat ringannya reaksi, makin berat makin tinggi dosisnya, biasanya
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3. Untuk tungkai t ungkai lakukan
peregangan otot-otot
tungkai bagian
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Trusted by over 1 million members
Try Scribd FREE for 30 days to access over 125 million titles without ads or interruptions! Start Free Trial Cancel Anytime.
Trusted by over 1 million members
Try Scribd FREE for 30 days to access over 125 million titles without ads or interruptions! Start Free Trial Cancel Anytime.
Trusted by over 1 million members
Try Scribd FREE for 30 days to access over 125 million titles without ads or interruptions! Start Free Trial Cancel Anytime.
Trusted by over 1 million members
Try Scribd FREE for 30 days to access over 125 million titles without ads or interruptions! Start Free Trial Cancel Anytime.
Trusted by over 1 million members
Try Scribd FREE for 30 days to access over 125 million titles without ads or interruptions! Start Free Trial Cancel Anytime.
Trusted by over 1 million members
Try Scribd FREE for 30 days to access over 125 million titles without ads or interruptions! Start Free Trial Cancel Anytime.
Trusted by over 1 million members
Try Scribd FREE for 30 days to access over 125 million titles without ads or interruptions! Start Free Trial Cancel Anytime.
Trusted by over 1 million members
Try Scribd FREE for 30 days to access over 125 million titles without ads or interruptions! Start Free Trial Cancel Anytime.
Trusted by over 1 million members
Try Scribd FREE for 30 days to access over 125 million titles without ads or interruptions! Start Free Trial Cancel Anytime.
Trusted by over 1 million members
Try Scribd FREE for 30 days to access over 125 million titles without ads or interruptions! Start Free Trial Cancel Anytime.
Trusted by over 1 million members
Try Scribd FREE for 30 days to access over 125 million titles without ads or interruptions! Start Free Trial Cancel Anytime.