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Slide 1 :
VIRAL HEPATITITS DR Kennedy kumar
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Hepatitis viruses Hepatitis Viruses - A,B,C,D,E Other viruses – Cytomegalo, EBV, HSV, Yellow fever, Rubella, Enteroviruses etc
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Viral hepatitis 50% of children do not develop Jaundice. Large tender liver is common. 30% will have splenomegaly Coagulation is usually normal
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Icteric Phase Liver is enlarged,tender Cervical adenopathy(10-20%) Splenomegaly(10-20%) Fever is absent Encephalopathy :Irritability Letargy,confusion
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Icteric Phase Clinical jaundice Dark urine:1-5 days before jaundice Patient may feel better Resolution of fever pruritus
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Pathology Infiltration of mononuclear cells Hepatic cells necrosis Kupfer cells hyperplasia Variable degrees of cholestasis In more severe cases; Bridging necrosis
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Laboratory Findings Serum bilirubin:5-20 mg/dl due to cholestasis, abnormal biliary flow at the canalicular level Direct bil =indirect bil SGOT,SGPT=400-4000 iu due to cytopathic injury Alk.phosphatase :mild elevation Synthetic function PT is usually normal: in severe hepatitis,PT is prolonged serum albumin hypoglycemia
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Hepatitis A (HAV) Picornavirus (RNA virus) Enterically transmitted (fecal/oral route) Often referred to as “infectious hepatitis” Only a single serotype exists Estimated to be the cause of 40% of acute hepatitis cases
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Hepatitis A Virus Transmission Close personal contact(e.g., household contact, child day care centers) Contaminated food, water (e.g., infected food handlers, raw shellfish) Blood exposure (rare)(e.g., injecting drug use, transfusion)
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Persons At Risk of Infection Household contacts of infected persons Persons, especially children, living in areas with increased rates of hepatitis Persons travelling to countries where hepatitis A is common Sex contacts of infected persons
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Hepatitis A - Clinical Features Incubation period average-30 days Range 15-50 days Route of spread - Ingestion Complications: 1)Fulminanthepatitis2)Cholestatic hepatitis3)Relapsing hepatitis Chronic sequelae: None
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Clinical features Jaundice Fatigue Abdominal pain Loss of appetite Nausea Diarrhoea Fever
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Laboratory Diagnosis Acute infection is diagnosed by the detection of HAV-IgM in serum by EIA. Past Infection i.e. immunity is determined by the detection of HAV-IgG by EIA.
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Treatment/Prevention (HAV) Interruption of fecal-oral spread Avoidance of contaminated water or food (undercooked shell fish) Proper handwashing in day care and healthcare facilities Prophylaxis with immune globulin before or early in incubation (< 2wks post exposure) is 80 - 90% effective Killed vaccine is available for those at risk. Safe and effective formalin inactivated deployed cell grown vaccine, 2 IM doses at 2-4 week intervals
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Hepatitis B Virus Viruses highly infectious as little as 0.00001 ml can transmit the disease
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Epidemiology Endemic throughout the world More than 2 billion people have infection and around 350 million are chronic carriers Every year 14-16 million people are infected and 2 lakh deaths occur In India - 43-45 million HBsAg carriers among which 10-12 million have HBeAg
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Hepatitis B Virus Serum hepatitis Incubation period-6wks to 6months 5-15% of cases go in for carrier state Persistent infection leads to CAH and Ca liver Chronic infection: <5 yrs, 30%-90% >5 yrs, 2%-10% Premature mortality fromchronic liver disease-15%-25%
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Routes of transmission 1 Perinatal transmission A carrier mother usually transmits hepatitis B virus to an infant perinatally 2 Blood contact Blood transfusion accidental contact with an infected person's blood or body fluids through skin cuts, abrasion, or mucosal membranes of the eyes and mouths. Sharing injection instruments for drug injection. Using contaminated instruments for ear piercing, tattooing or acupuncture. Sharing personal items such as razors, shavers or nail trimmer which may have been contaminated with blood 3 Sexual contact Unprotected sexual contact with a carrier
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Viral Markers HBV – Dane particle HBsAg-Australia Ag Three types one group specific Ag Alpha and two pairs of type specific Ags d-y and w-r (ayw,ayr,adw and adr) Appears in the blood after a month and peak levels seen in pre icteric phase. Anti HBsAg appears within a week of disappearance of surface Ag
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Viral Markers HBcAg –not detactable in serum but demonstrated in liver by IF Anti HBcAg appears in the preicteric phase HBeAg – hidden antigenic component of the virus core. Appears in the same time as HBsAg but disappears soon.Directly proportional with the no of viral particles and degree of infectivity Anti Hbe-appears after the disappearance of Ag
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Spectrum of Chronic Hepatitis B Diseases 1Chronic Persistent Hepatitis - asymptomatic 2. Chronic Active Hepatitis - symptomatic exacerbations of hepatitis 3. Cirrhosis of Liver 4. Hepatocellular Carcinoma
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Hepatitis B carriers Two categories based on serological markers. Super carriers – HBeAg in blood – highly infectious. - Very minute amounts of serum or blood from such carriers can transmit the infection. - Have high titres of HBsAg and DNA polymerase and mildly raised serum transminase levels - HBV may be demonstrable in their blood. Simple carriers – more common type – no HBeAg. - low level of HBsAg - HBV and DNA polymerase are absent. - transmit the infection only when large volumes of blood or serum are transferred – blood transfusion.
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Clinical Features IP 2-6 months Onset insidious, fever is not prominent Rash,arthralgia, polyarthritis nodosa and glomerulonephritis Some progress to chronic active hepatitis and cirrhosis Primary hepatocellular Ca – late consequence Case fatality 0.5 –2 %
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Lab diagnosis Serum markers. The Ags and Abs are detected in the serum by ELISA,CIE,CF,RIA etc HBsAg - used as a general marker of infection. HBsAb - used to document recovery and/or immunity to HBV infection. Anti-HBc IgM - marker of acute infection. Anti-HBcIgG - past or chronic infection.
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Lab diagnosis HBeAg - indicates active replication of virus and therefore infectiveness. Anti-Hbe - virus no longer replicating. However, the patient can still be positive for HBsAg which is made by integrated HBV. HBV-DNA - indicates active replication of virus, more accurate than HBeAg especially in cases of escape mutants. Used mainly for monitoring response to therapy.Detected by PCR
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Treatment Interferon - for HBeAg +ve carriers with chronic active hepatitis. Response rate is 30 to 40%. Lamivudine - a nucleoside analogue reverse transcriptase inhibitor. Well tolerated, most patients will respond favorably. However, tendency to relapse on cessation of treatment. Another problem is the rapid emergence of drug resistance. Successful response to treatment will result in the disappearance of HBsAg, HBV-DNA, and seroconversion to HBeAg.
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Prophylaxis-Vaccination Recombinant vaccine Three doses for both children and adults. 1ml for adults and 0.5ml for children 0,1 and 6 months is the dosage schedule
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Prophylaxis HepatitiBImmunoglobulin – (HBIG 200units/ml) used to protect persons who are exposed to hepatitis B within 48 hours of the incident and also can be given to neonates whose mothers are HBsAg and HBeAg positive.0.5ml IM Other measures - Screening of blood donors, blood and body fluid precautions
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Hepatitis C Virus Enveloped single stranded RNA virus Common cause of post transfusion hepatitis Resembles type B hepatitis in clinical and epidemiological features Inc period – average 50days About 150million carriers seen in worldwide
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Risk Factors Associated with Transmission of HCV Transfusion or transplant from infected donor Injecting drug use Hemodialysis (yrs on treatment) Accidental injuries with needles/sharps Sexual/household exposure to anti-HCV-positive contact Multiple sex partners Birth to HCV-infected mother
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Laboratory Diagnosis HCV antibody To diagnose hepatitis C infection. Not useful in the acute phase as it takes at least 4 weeks after infection before antibody appears. HCV-RNA PCR and branched DNA. To diagnose HCV infection in the acute phase. However, its main use is in monitoring the response to antiviral therapy. HCV-antigen - EIA
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Treatment Interferon For patients with chronic active hepatitis. The response rate is around 50% 50% of responders will relapse upon withdrawal of treatment. Ribavirin - Combination of interferon and ribavirin is more effective than interferon alone.
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Prevention of Hepatitis C Screening of blood, organ, tissue donors High-risk behavior modification Blood and body fluid precautions
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? antigen HBsAg RNA Hepatitis D (Delta) Virus
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Hepatitis D Virus Modes of Transmission Percutanous exposures injecting drug abusers Permucosal exposures sex contact
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Hepatitis D - Prevention HBV-HDV Co infection Pre or post exposure prophylaxis to prevent HBV infection. HBV-HDV Super infection Education to reduce risk behaviors among persons with chronic HBV infection.
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Hepatitis E Virus Spherical non enveloped single stranded RNA virus Resembles HAV in clinical course Often appears as epidemics Inc per – average 6 weeks Mild and self limited
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Hepatitis E - Epidemiological Features Most outbreaks associated with faecally contaminated drinking water. Several other large epidemics have in the Indian subcontinent and the USSR, China, Africa and Mexico. In the United States and other nonendemic areas, a low prevalence of anti-HEV (<2%) has been found in healthy populations. The source of infection for these persons is unknown. Minimal person-to-person transmission.
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Hepatitis E - Clinical Features Incubation period: Average 40 days Range 15-60 days Case-fatality rate: Overall, 1%-3% Pregnant women, 15% - 25% Illness severity: Increased with age Chronic sequelae: None identified
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Prevention and Control Measures for Travelers to HEV-Endemic Regions Avoid drinking water (and beverages with ice) of unknown purity, uncooked shellfish, and uncooked fruit/vegetables IG prepared from donors in Western countries does not prevent infection. Unknown efficacy of IG prepared from donors in endemic areas.
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Comparison of Hepatitis Viruses
Acute Hepatitis B Wh...
Hepatitis B and Live...
Kawasaki disease pre...
Hepatitis C in pregnancy
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Hepatitis A - E
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