EPIDEMIOLOGI HEPATITIS VIRUS

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PENDAHULUAN Hepatitis virus adalah suatu penyakit yang disebabkan oleh virus hepatitis A (VHA), virus hepatitis B (VHB) dan virus hepatitis Non-A Non-B(VHNANB) al. VHC, VHD, VHE Klinis dikenal sejak Hipocrates

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Sebagai etiologi,VHA dan VHB baru diketahui pada awal abad 19, VHNANB baru pada l974, Prince dkk. 1965, Blumberg menemukan antigen Australia (AuAg)

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Hepatitis virus B lebih penting ok: Disamping ada pend. simptomatik, terdapat juga yang asimptomatik (karier) sebagai sumber penularan 5-10% kronik, sirosis hepatis dan karsinoma hepatoseluler

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1%.5% Di beberapa negara mencapai 17% 5 .5 ± 9.Virus hepatitis B diperkirakan meng infeksi 2 miliar manusia Lebih 300 juta penduduk dunia men derita infeksi kronik Di Indonesia prevalensi HBsAg 3. rata-rata 5.

1% di seluruh Indonesia Diperkirakan akan meningkat cepat. seiring dengan maraknya penyalah gunaan narkotika 6 .Hepatitis C saat ini berada ditempat kedua sebagai penyebab hepatitis kronik Prevalensinya 2.

Hepatitis A (1) Definition A small enveloped symmetrical RNA virus sharing many of the properties of the picornavirus family and the cause of infectious or epidemic hepatitis transmitted by the fecal-oral route 7 .

Hepatitis A (2) Epidemiology Occurs endemically in all parts of the world Under reported as many cases are asymtomatic and anicteric Prevelence is decreasing in many industrialized countries Incubation period os 3-5 weeks with a mean of 28 days 8 .

Hepatitis A (3) Spread by the fecal-oral route with outbreaks common where there is poor sanitation and overcrowding No risk factor identified in 40% cases Replicates principally in the gut and is only transiently present in the serum so that parenteral transmission is rare 9 .

chills. fatigue etc.Hepatitis A (4) Clinical Course Infection in under 2-year-olds is very mild with few symptoms In adults leads to symptomatic infection in 76% to 97% patients Frequently heralded by non-spesific symptoms: fever. headaches. 10 .

Hepatitis A (5) Followed by anorexia. vomiting and right upper quadrant pain Jaundice. dark coloured urine and clay coloured stools develop Jaundice lasts for 1-2 weeks. At this stage my be impossible to distinguish from other forms of hepatitis 11 .

Hepatitis A (6) Recovery over 2 months Rarely fulminant (0.14%) No risk of malignancy 12 .

Hepatitis A (7) Diagnosis Spesific serological marker anti-HAV IgM detectable in serum for 45-50 days after onset of symptoms Need to also do marker for hepatitis B 13 .

Hepatitis A (8) Treatment By the time jaundice appears viral shedding has ceased so patient does not need to be isolated Immunoglobulin (Ig) can prevent and attenuate HAV infection HAV vaccine used in trials produces seroconversion rate of 90-100% 14 .

Hepatitis B (1) Definition A double stranded DNA virus requiring reverse transcriptase for its replication 15 .

Hepatitis B (2) Epidemiology Mode of transmission varies from country to country Far East Asia: infected during childhood and 15% to 20% are chronic carriers with persistence of significant amount of HBsAg in the serum 16 .

Hepatitis B (3) Western countries: transmission during sexually active years as a sexually transmitted disease. especialy in male homosexuals. contaminated syringe needles and intravenous drug abusers Incubation period of 4 to 26 weeks 17 .

Hepatitis B (4) Clinical As with most of the viral hepatitis it may be impossible to distinguish from other viral hepatitidies Symptoms and sign less evident in children (9% <4 years of age) than in adults (33% >30 years old) Extrahepatic manifestations of rash and arthralgia are common 18 .

Hepatitis B (5) Most serological tests are reliable: Act or Chr Recov Post vacc HBsAg + antiHBc + + antiHBs + + 19 .

Hepatitis B (6) Prognosis 10% to 20% develop chronic infection 200x risk of malignancy Treatment Alpha and gamma interferon used in chronic disease states but should not be used outside well controlled clinical trials 20 .

Hepatitis B (7) Prevention Immunoprophylaxis using noninfectious HBsAg particles and recombinant tehnology Candidates for prophylaxis: Health workers frequently exposed to blood product IV drug users who are HBsAg -ve 21 .

Hepatitis B (8) Candidates for prophylaxis: Patients with multiple transfusion Neonates of HBsAg +ve mothers Travellers to endemic areas for prolonged stays Institutionalized persons Promiscuous population (2) 22 .

Hepatitis C (1) Definition As enveloped single stranded RNA virus which seems to be distantly related to the flavivirus and responsible for most of the cases of transfusion acquired non-A. non-B hepatitis 23 .

of all cases of post transfusion hepatitis. if not all.Hepatitis C (2) Epidemiology Most. non-B are due to this virus In 30% to 50% cases no route of infection is found and infection is considered sporadic 24 . previously termed non-A.

Hepatitis C (3) Little evidence of perinatal transmission Sexual transmission still awaiting confirmation Risk factors: Low socioeconomic/educational level x3 Household/sexual contacts x6 Multiple sexual partners x11 25 .

Hepatitis C (4) Clinical Profile Acute hepatitis C a mild illness. 75% anicteric and asymptomatic Fulminant cases rare Extra-hepatic manifestations rare ± possible link to aplastic anemia Hallmark is that of chronic persistent infection 26 .

Hepatitis C (5) Clinical Profile 50% infected patients develop clinical and biochemical evidence of chronic infection 20% cases heve cirrhosis but few clinical manifestations (2) 27 .

Liver function test should be performed plus referal to a hepatologist 28 .Hepatitis C (6) Diagnosis Ortho anti-HCV test popular but have high false-positivity A positive test should be followed by radioimmunolabeled blotting assay (RIBA) and neutralization test in experienced laboratories.

The two differing strains may require designation HCV-1 and HCV-2 29 .Hepatitis C (2) (7) Diagnosis The virus has diferrent genomic sequences depending on the geographical location (Japan vs USA) so a test developed for one genome may not identify it in another region.

Hepatitis C (8) Prognosis 50% develop chronic infection 20% develop cirrhosis Possible association with hepatocelluler carcinoma 30 .

Hepatitis C (9) Treatment Recombinant interferon has fair success but is associated with a high relapse rate and is expensive to use Oral Ribavirin used in some patient with similar results 31 .

Hepatitis D (delta hepatitis) (1) Definition A defective RNA virus which requires the presence of hepatitis B to succesfully replicate 32 .

Hepatitis D (delta hepatitis) (2) Epidemiology Co-infects the patient at the same time with HBV or from superinfection once HBV is established Common in Southern Europa and Middle East In Western countries associated with iv drug abuse 33 .

Hepatitis D (delta hepatitis) (3) Clinical Profile If co-infection with HBV the masked by that virus Superinfection leads to a relaps or ³flare up´ of chronic hepatitis Rarely fulminant hepatitis In liver transplant replication of HDV without HBV replication may have a milder course than replication of HBV and HDV 34 .

Hepatitis D (delta hepatitis) (4) Diagnosis Determination of HDAg by enzymeimmunoassay is best marker of acute HDV infection HDAg may also be present intermittently in chronic infection Must also test for HIV. HBV and HCV as most patients in Western countries with HDV are iv drug users 35 .

Hepatitis D (delta hepatitis) (5) Complications HBsAg +ve patients with HDV superinfection may develop cirrhosis and HCV at an earlier age than HBsAg carriers May cause a more rapidly progressive disease in HBV +ve patients 36 .

Hepatitis D (delta hepatitis) (6) Treatment There are ongoing studies concerning the use of interferon but these have been associated with relapse and a poor success rate 37 .

nonB hepatitis due to unenveloped single stranded RNA virus 38 .Hepatitis E (1) Definition An enterically transmitted non-A.

Hepatitis E (2) Epidemiology May occur in epidemic and sporadic forms Associated with drinking water contaminated by sewage Infection among household contacts that person to person spread may occur 39 .

Hepatitis E (3) Epidemiology Outbreaks in Southeast Asia. Mexico. Indian subcontinent. Africa. Central America and Ethiopia where peaks may occur every 2-3 years Virus similar to the calciviruses (such as Norwalk virus) which are normally associated with severe diarhea (2) 40 .

Hepatitis E (4) Epidemiology Viral particles in feces 28-45 days after exposure and 9 days before clinical onset of symptoms (3) 41 .

4%.Hepatitis E (5) Clinical Presentation Malaise 99.3%. Abdominal tenderness 82%. Vomiting 93.0%.1% 42 . Clay colour stools 36. Nausea 99.5%. Headache 96.5%.6%.5%. Anorexia 99. Dark urine 94. Fever 97. Jaundice 100%.

Hepatitis E (6) Diagnosis Fluorescent antibody blocking test not yet commercially available 43 .

Hepatitis E (7) Prognosis Usually excellent with good recovery In pregnant women may be associated with 20% mortality Use of immunoglobulin not determined 44 .

Sebab Secara epidemiologis semua jenis hepatitis virus tidak membutuhkan vektor dalam penyebarannya 45 .Soal No 1 Secara epidemiologis semua jenis hepatitis virus mempunyai pola penyebaran yang sama.

sirosis dan karsinoma 46 .Soal No 2 Saat ini semua jenis hepatitis virus merupakan problema kesehatan masyarakat di Indonesia Sebab Semua jenis hepatitis virus dapat berkembang menjadi kronis.

Soal No 3 Hepatitis virus A tidak termasuk salah satu penyakit karantina Sebab Hepatitis virus A termasuk salah satu penyakit yang tidak mempunyai potensi wabah 47 .

dan ibu hamil kepada bayinya. 48 .Soal No 4 Penularan semua penyakit hepatitis virus dapat secara vertikal dan horisontal Sebab Penularan semua penyakit hepatitis virus dapat melalui penderita. karier. hubungan seksual.

Soal No 5 Secara epidemiologis program pemberantasan hepatitis virus B di Indonesia sulit berhasil Sebab Secara epidemiologis pada hepatitis virus B dikenal kelompok asimtomatik dan karier 49 .

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