HEPATITIS

Infeksi virus termasuk virus hepatitis

Alkoholism

Keracunan

Malaria
Kurang gizi

VIRUS
 Organisme

terkecil dengan ukuran

20-40 nm
 Terdiri dari Core ( inti), Capsid
(selubung) dan Envelope (kapsul)
 Mengandung satu jenis asam nukleat
(RNA/DNA)
 Hidup dan bereplikasi tergantung
pada sel pejamu ( host)

Penyebab hepatitis
 Virus

Hepatitis A

 Virus

Hepatitis G

 Virus

Hepatitis B

 Virus

Hepatitis TT

 Virus

Hepatitis C

 Virus

hepatitis lain

 Virus

Hepatitis D

 Penyakit

 Virus

Hepatitis E

 Obat,

autoimun

racun

Afrika selatan dan Asia Hepatitis D virus Delta virus (HDV) Parenteral Akut dan kronik= HBV. sporadis tiap 5-10 thn Asia timur Hepatitis B virusHepatitis SerumParenteral. epidemis lokal Belum ada Utara dan Mexico sporadis tiap 5-10 thn Hepatitis G virus (HGV) Parenteral Akut dan kronik Belum jelas Belum jelas Belum ada . Amerika HCV kronik selatan. tergantung dari essential daerahnya Hepatitis E virus (HEV) Enteral Hanya akut Epidemis di Asia. banyak di Rusia 10 . Akut dan kronikAfrika dan Asia timur >>350 . sedang170 juta pengidap Belum ada (HCV) Non B sexual (50-70%) di Eropa timur.400 juta pengidap Ada (HBV) sexual (5-10%) Sebagian Kanada dan HBV kronik Amerika Selatan Hepatitis C virusHepatitis Non A -Parenteral. bervariasi. Timur tengah.60% pengidap HBV Ada (=HBV) HBV ko-faktor yg (5-10%) kronik. vertikal.Jenis-jenis Hepatitis Virus VIRUS NAMA LAIN PENULARAN Hepatitis A virus Hepatitis Infeksiosa (HAV) Enteral INFEKSI DISTRIBUSI GEOGRAFIK PREVALENSI VAKSIN Hanya akut Afrika >>. epidemis lokalAda Amerika Selatan. vertikal Akut dan kronik Timur tengah >>. Afrika Bervariasi.

Hepatitis C: “Sleeping with the Enemy” (musuh dalam selimut) .

Statistik Global • 170 juta terinfeksi • Global: 3% Sumber: WHO Fact Sheet No. 164 2000 .

164 2000 .Statistik Regional Indo: 7 juta Indonesia: 65 % Gen-1 Indonesia: Kawasan yang Angka Kejadiannya Tinggi (dibanding Eropa dan Amerika) Sumber: WHO Fact Sheet No.

high risk sexual practices .Virus Hepatitis C      Small. transfusion of blood and blood products. chronic haemodialysis. single-stranded RNA virus Family: Flaviviridae 6 major genotypes and > 50 subtypes HCV replicates preferentially in hepatocytes but is not directly cytopathic. enveloped. nosocomial transmission. leading to persistent infection Infection due mainly to:  IVDU.

Perjalanan penyakit Hepatitis C .

Cara Penularan Hepatitis C .

tenaga laboratorium) .Kelompok Risiko Tinggi Infeksi HCV        Pengguna Narkoba suntik (risiko amat tinggi) Penerima transfusi darah yang tidak diskrining (amat tinggi) Pengguna alat kesehatan (jarum. Perawat. pisau. Bidan. Dokter gigi. Cangkok Organ Pekerja Kesehatan (Dokter. sunat dengan alat yang tidak steril. Berhubungan seks dengan partner yang terinfeksi (baik heteroseksual ataupun homoseksual) tanpa pengaman Pasien Cuci Darah. tato. gunting) yang tidak disterilkan sempurna dan pasiennya Ditindik.

Hepatitis B .

 Terdapat 350 juta penderita Hepatitis B kronis didunia.  Frekwensi 3-18 % tersebar diseluruh Indonesia.  Indonesia termasuk daerah dengan endemis sedang-tinggi.HEPATITIS B  Penyakit peradangan hati yang disebabkan Virus Hepatitis B. .

Prevalensi Global Hepatitis B World prevalence of HBV carriers HBsAg carriers – prevalence <2% 2–7% >8% Poorly documented WHO 2003 .

Gambaran Skematis Virus Hepatitis B DNA polymerase Inner protein core (HBcAg) HBV DNA Outer lipoprotein envelope containing HB surface antigen HBsAg HBeAg .

Electron Micrograph of the Hepatitis B Virus The photograph shows Dane particles. spheres and filaments .

Double-stranded HBV DNA 4. Synthesis of L (-) strand by reverse transcriptase . Fusion 3. Endoplasmic reticulum 7. Supercoiled DNA 6. Assembly of complete cores 2.Siklus Hidup Virus Hepatitis B 1. Transcription of L (-) strand 5. Synthesis of core proteins 8.

Cara Penularan Hepatitis B • The hepatitis B virus is present in all body fluids of infected individuals • Modes of transmission: – – – – – – Perinatal/vertical Horizontal Sexual contact Contaminated blood and blood products Organ/tissue transplantation Re-use of unsterilised needles and syringes WHO 2003 .

Perjalanan Penyakit Hepatitis B Acute HBV infection 90–95% neonatal infection 50% childhood infection Fatal Chronic 15–40%* progressive HBV liver failure infection 5–10% adult infection ~2% Fulminant hepatic failure Cirrhosis Decompensated cirrhosis HCC Death *Lok et al 2002 .

Genome DNA virus. Dapat ada pada hepatitis B akut maupun kronik dan hepatitis B tipe “ wild” maupun “mutant” 2. Penanda supresi virus yang menetap. Anti HBe terjadinya dan tidak dijumpai pada tipe mutan Antibodi terhadap HBeAg. Penanda awal . HBsAg pada hepatitis B tipe mutant.Penanda virus Hepatitis B kronik (i) Tes 1. Dapat dijumpai 4. penanda replikasi virus. HBeAg virus. penanda replikasi Dapat ada pada hepatitis B akut maupun kronik 3. HBV DNA Arti klinis Genom DNA virus. Protein virus.

telah sembuh dan kebal terhadap hepatitis B. Anti HBs Penanda 6. Infeksi akut (IgM) dan infeksi kronik (IgG) . Penanda pernah terinfeksi hepatitis B.Penanda virus Hepatitis B kronik (ii) Tes 5. Anti HBc Arti klinis Antibodi terhadap HBsAg . Antibodi terhadap HBcAg.

Makna Marker Serum pada Infeksi Hepatitis B .

Hepatitis akut Hepatitis berjalan singkat. tubuh menghilangkan virus dalam waktu 6 bulan Hepatitis kronik Penyakit berlansung lebih dari 6 bulan karena tubuh tak mampu menghilangkan virus .

Hepatitis B Akut .

Hepatitis B Kronik .

~ #% (170 million persons) Risk of chronicity (variable) – 75%-85% Early fibrosis progression rate – Low Risk of cirrhosis – Up to 10% within 20 years. 20% within 30 years Cirrhosis-related mortality – 1% .HCV Infection: “The Facts”       Estimated global pravalence -.5%/years Incidence of HCC in patients with cirrhosis – 1% .4%/year .

Projection of lifetime outcomes in HCV infection Infection Acute stage 20% 80% Chronic hepatitis Resolved 20% 80% Stable -20% Cirrhosis Decompensation ~75% Slowly progressive 1-4% Per year HCC .

chronic haemodialysis.HCV  Small. single-stranded RNA virus  Family : Flaviviridae  Hypervariable regions at E1 and E2 domains  6 major genotypes and >50 subtypes  HCV replicates preferentially in hepatocytes but is not directly cytopathic. transfusion of blood and blood products. enveloped. nosocomial transmission. high . leading to persistent infection  Infection due mainly to:  IVDU.

Hepatitis C virus: structure RNA genome Envelope Nucleocapsid (core) protein .

HCV Life Cycle Translation and Polyprotein processing Membrane fusion Endocytosis Virion assembly And maturation Uncoating RNA replication + strands Vesicle fusion and Virion release strands .

Acute Viral Hepatitis  Hepatitis Virus Infections : The most common cause of liver disease  Many Hepatitis episodes :aninteric. inapparent. viral hepatitis is the major cause of persistent viremia . or subclinical  Glorally.

The agents of viral hepatitis : classified into two groups Enterically transmitted    Hepatitis A Virus (HAV) Hepatitis E Virus(HEV) Possibly third agent (? HFV) Blood Borne Agents  Hepatitis B Virus (HBV)  Hepatitis D Virus (HDV)  Hepatitis C Virus (HCV)  Hepatitis G Virus (HGV) .

HEV.HAV. and etc  are non enveloped viruses  Survive intact when exposed to bile  Shed in feces  Not linked to chronic liver disease Don’t result in a viremic or intestinal carrier state .

HDV and HGV are :  Enveloped viruses  Disrupted by exposure to bile / detergents  Not sheld in feces  Linked to chronic liver diseases  Associated with persistent viremia . HCV.HBV.

Model of the Hepatitis B Virus .

Model of the Hepatitis C Virus .

IgM Anti-HEV --- 0.5 – 1.-1 14-60 d (40 d) ? Transmission . E.. circular RNA single strand.0% 0. D. G Hepatitis A B C D E G Picornavirus Hepadnavirus flavivirus Viroid Calicivirus Flavivirus ? 27-32 nm 42 nm ? 36 nm 27-32 nm ? Nucleic acid RNA single strand. IgM Anti-HDV Anti-HDV. linear Incubation period (mean) 14-45 d (30d) 30-180 d(70 d) 14-180 d (50 d) .1% 1% 5-30%? 10% ? ? Yes (? %) Active immun Yes Yes No No No No Passive immun yes yes No No No ? No Family  Antibodies Fulminant hepatitis Healing acute Hepatitis . B. linear RNA single strand.001-0. linear DNA double strand. HBeAg --- HDAg HEAg --- Anti-HAV Anti-HAV.5-1. circular RNA single strand.fecal-oral route Yes No No No yes No -Blood No Yes yes yes No -Vertically No Yes yes yes No ? -Sexually No Yes yes yes No ? Antigens HAAg HBsAg. IgM Anti-HBs Anti-HBe Anti-HBc Anti-HCV Anti-HCV.5% 0.Virus Hepatitis A. C.0% 1-3-25% 2% (25%-?) ? >99% >90% 10-40% 50-80% >95% ? Chronic active Hepatitis 0% <10% (0. circular RNA single strand.5%) 30-90% (<10) 20-50% ? (<5%) Yes (? %) Liver cirrhosis <0.

Epidemiology and risk factors HAV           Incubation period : 15-50 days Worldwide distribution : highly endemic in developing countries HAV is excreted in the stools Viremia is short lived Prolonged fecal excretion Enteric Other risk factors include exposure No evidence for maternal-neonatal transmission Prevalence correlates with sanitary standards & large houseshold size Percutaneous transmission rare .

Epidemiology and risk factors HEV         Incubation period : 40 days Widely distributed : epidemic and endemic forms HEV RNA in serum and stool during acute phase The most common form of sporadic hepatitis A largely waterborne epidemic disease Intrafamilial. secondary cases are uncommon Maternal-neonatal transmission has been documented Prolonged viremia or fecal shedding unusual .

cervicovaginal secretions. cirrhosis. Persistent infection linked with chronic hepatitis. other body fluids. 90% of infected neonates.Epidemiology and risk factors HBV       Incubation period: 15 to 180 days (average 60-90 days) HBV viremia lasts for weeks to months after acute infection 1-5% of adults. semen. . and 50% of infants develop chronic infection and persistent viremia. hepatocellular carcinoma Worldwide distribution : HBV carrier prevalence >15% in Asia. saliva. HBV present in blood.

maternal-infant transmission No evidence for fecaloral spread .Modes of transmission Bloodborne  Recipients of multiple blood products  Injecting drug user  Hemodialysis patients  Health care and other workers exposed to blood Sexual transmission Tissue penetrations (percutaneous) or permucosal transfer  Needlestick accidents  Shared razoblades  Tattoo  Acupuncture  Shared toothbrushes Maternal-neonatal.

 HDV infections occur solely in individuals at risk for HBV infection (coinfections or superinfections)  Modes of transmission .Epidemiology and risk factors HDV  Incubation period : 4-7 weeks  Endemic in Mediterranean basin. European parts of former Soviet Union. Middle East. and Amazon basin.  Viremia short lived (acute infection) or prolonged (chronic infection). parts of Africa.

hepatocellular carcinoma  Modes of transmission .Epidemiology and risk factors HCV  Incubation period :15 to 160 days (major peak at about 50 days)  Prolonged viremia and persistent infection common : wide geographic distribution  Persistent infection linked with chronic hepatitis. cirrhosis.

Epidemiology and risk factors HGV  Incubation period uncertain  Prolonged viremia and persistent infection common  HGV RNA in 10 – 20% of patients with  Chronic hepatitis  Chronic hepatitis B  Chronic hepatitis C  Cryptogenic cirrhosis  Modes of transmission .

Insidensi KHS didunia sesuai distribusi geografik:  4 kategori  Insidensi tinggi 10-20 kasus per 100. Asia Tenggara insidensi tinggi Indonesia + 28.000 penduduk .000 penduduk  Insidensi sedang 5 – 9 kasus per 100.1 kasus/100.000 penduduk  Insidensi rendah <5 kasus per 100. Cina.000 penduduk Indonesia. Afrika Selatan.

Umum  Asia. Amerika > 60 tahun  Mozambiqua 25 – 34 tahun  500 kali lebih tinggi dibanding Amerika . Afrika 20 – 40 tahun  Eropa.

2%) dari 27954  Jakarta 296 (2.2%) dari 11193  Semarang 623 (2.9%) dari 7863  Bandung 189 (1.Frekuensi relatif KHS di Indonesia  Surabaya 582 (2.9%) dari 30345  Yogyakarta 123 (1.5% dari 7909  Padang 150 (1.6 tahun) 11279  Denpasar (325 (3%) dari 10558 Laki-laki : wanita : 4-6 : 1 .