ºÝºÝߣ

ºÝºÝߣShare a Scribd company logo

Hepatitis .pdf

•
•
Ashish Jitendranath
Ashish Jitendranath

This document discusses viruses that can cause hepatitis, focusing on hepatitis A, B, and E viruses. It provides details on the virology, pathogenesis, epidemiology, clinical features, diagnosis, prevention and treatment of hepatitis A, B and E. Key points include that hepatitis A virus is transmitted via the fecal-oral route and causes an acute, self-limiting infection, while hepatitis B and E viruses can cause both acute and chronic infections leading to cirrhosis or liver cancer if chronic infection is established. Vaccines exist for hepatitis A and B but not E.

1 of 22
VIRUSESCAUSING HEPATITIS DR ASHISH JITENDRANATH
Liver complex organ Hepatocytes are site of detoxi f ication and metabolism. Infections of liver tend to a ff ect either the cells, producing typical hepatocellular disorder or biliary tract, producing cholestasis and feature so of infection in hollow organ. Space occupying tend to produce biochemical changes of cholestasis, but rarely cause jaundice DR ASHISH JITENDRANATH INTRODUCTION
VIRALINFECTIONSOFLIVER • Hepatitis A virus • Hepatitis E virus • Hepatitis B virus • Delta Virus • Hepatitis C virus • Hepatitis G virus • Transfusion transmitted virus • Epsterin Barr virus • Cytomegalovirus • Yellow virus
HEPATITISA
INTRODUCTION Worldwide distributions especially in high dense populations Spreads among children. Outbreak in adults is not common 1% may su ff er serious life threatening disease Immunity lifelong. 3 pattern of disease- Sporadic among adults, epidemic in school children and Explosive common source outbreaks. Feco oral route and also by ingestion of contaminated food Virus excretion in feces may be 2 weeks before to 2 weeks after appearance of jaundice.
VIROLOGYANDPATHOGENESIS Small RNA virus 27 nm in diameter with ss positive sense RNA. 4 capsids polypeptides are present Vp1-4. One major serotype and 4 subtypes de f ined on basis of sequence of VP1/2 junction Hepatic damage occurs after feverish stage of illness and is probably immunologically mediated. Neutralising antibodies are directed against groups of closely clustered epitopes on virus surface. Humans are only natural host.
CLINICALFEATURES IP 15-45 days. Malaise, nausea, lassitude, myalgia, arthralgia and variable fever. Intestinal mucosa is in f lamed at this stage and loose stools are passed. Viruses excreted in stool and urine. Urine darkens as bilirubinuria increases and stools may be pale. Jaundice is f irst seen in sclerae and later skin. Fever resolves and virus excretion ceases as jaundice developed
CLINICALFEATURES Patients are now no longer infectious and most feel better. After 7-10 days appetite returns and jaundice resolve No chronic or carrier stage. Complication is liver failure
DIAGNOSIS Clinical suspcion Rule out other so send panel to con f irm Demonstration of speci f ic IgM by antibody capture EIA. Peak 2 weeks after elevation of liver negzymes and disappear within 3-6 months Ig G after Igm and persist for decades PCR HAV antigen detection
PREVENTIONANDTREATMENT General hygiene No speci f ic antiviral treatement 2 vaccines 1. Formaldehyde inactivated vaccine 2. Live attenuated vaccine Also Human immunoglobulin for post exposure prophylaxis of intimate contacts
HEPATITSB
INTRODUCTION Chronic infection with liver in f lammation leading eventually to cirrhosis and malignant change in liver. Vertical and horizontal infection from mother to child can produce successive generations pop chronically infected, infectious carriers
VIROLOGYANDPATHOGENESIS Small enveloped virus containing partially ds DNA. 3 morphological forms- Spherical, tubular and Complete form. DNA contains 4 major genes that each encode more than one protein. Surface protein gene encodes 3 polypeptides including HBsAg make up the viral envelope C gene encodes core or capsid proteins and Precore protein. P gene encodes reverse transcriptase and RNAase and X gene encodes transactivator proteins. HBsAg is major protein of hep b virus. Major antigenic determinant is a antigen, antibodies to which confer protection after infection or vaccination.
VIROLOGYANDPATHOGENESIS 2 pairs of mutually exclusive sub determinants- d or y, and w or r- giving 4 phenotypes add, add, aye and ayr. HBC Ag is major nucleocapsid antigen. HBeAg is cleavage product of HBcAg and is a marker in blood for HBV replication. Mutations in precore region of HBV causes faulty HBeAg. Around half of chronically infected HBsAg positive and HBeAg Nega posses this mutation.
VIROLOGYANDPATHOGENESIS Mechanism of binding to cell not known. Most studies suggest virus not cytotoxic. 10% of patients persistent infection causes chronic hepatitis progressing to cirrhosis after 30 years. Persistent infection is thought to result from failure of initial immune response. Liver carcinoma 100 fold excess risk. Hep b gets incorporated into host chromosome but most of the viral genes are truncated
EPIDEMIOLOGY Risk group 1. Iv drug users 2. Homosexual men 3. Sexual contacts of antigen positive persons 4. Residents in long stay homes for mentally handicapped people 5. Renal dialysis patients 6. Recipients of multiple blood products 7. Surgeons dentists 8. Infants of positive mothers
EPIDEMIOLOGY Global HBV prevalence in HIV infected persons is 7.4% Presence of HIV greatly enhances risk of developing HBV associated cirrhosis and liver cancer
CLINICALFEATURES IP 3-6 months. Upto 90% of cases are subclinical. Prodromal symptoms are followed by afebrile jaundice similar to that of HepA.. Prodrome Mild arthritis and faint rash. Clinically di ff icult to distinguish acute hepatitis. Patients with serum HBV DNA levels above 1000 are considered infectious why blood borne route. 5-10% patients become chronically infected. Leading to Cirrhosis and hepatocellular carcinoma.
LABDIAGNOSIS • Antigen markers • HBsAg- First marker to appear • HBeAg- Indicates active viral replication and high infectivity • HBcAg- Not detected. Can be detected in hepatocytes • Antibody markers • AntiHBcAb- IgM indicates acute hepatitis and IgG appears in chronic hepatitis • AntiHBsAb marker o recovery or Vaccination • AntiHBeAb- indicates low viral replication and low infectivity. • Molecular markers. HBV DNA detection. Indicates active viral replication and high infectivity. Monitoring plays a load in treatment. • Non speci f ic markers- Liver enzymes
Hepatitis .pdf
TREATMENT Tenofovir and Telbivudine are the agent of choice Tenofovir and emtricitabine for HIV Other drugs lamivudine and peg interferon
VACCINATIONS Active immunisations. Recombinant sub unit using surface antigen in bakers yeast by DNA recombinant technology Passive immunization - Hep b immunoglobulin

More Related Content

Hepatitis .pdf

  • 2. Liver complex organ Hepatocytes are site of detoxi f ication and metabolism. Infections of liver tend to a ff ect either the cells, producing typical hepatocellular disorder or biliary tract, producing cholestasis and feature so of infection in hollow organ. Space occupying tend to produce biochemical changes of cholestasis, but rarely cause jaundice DR ASHISH JITENDRANATH INTRODUCTION
  • 3. VIRALINFECTIONSOFLIVER • Hepatitis A virus • Hepatitis E virus • Hepatitis B virus • Delta Virus • Hepatitis C virus • Hepatitis G virus • Transfusion transmitted virus • Epsterin Barr virus • Cytomegalovirus • Yellow virus
  • 5. INTRODUCTION Worldwide distributions especially in high dense populations Spreads among children. Outbreak in adults is not common 1% may su ff er serious life threatening disease Immunity lifelong. 3 pattern of disease- Sporadic among adults, epidemic in school children and Explosive common source outbreaks. Feco oral route and also by ingestion of contaminated food Virus excretion in feces may be 2 weeks before to 2 weeks after appearance of jaundice.
  • 6. VIROLOGYANDPATHOGENESIS Small RNA virus 27 nm in diameter with ss positive sense RNA. 4 capsids polypeptides are present Vp1-4. One major serotype and 4 subtypes de f ined on basis of sequence of VP1/2 junction Hepatic damage occurs after feverish stage of illness and is probably immunologically mediated. Neutralising antibodies are directed against groups of closely clustered epitopes on virus surface. Humans are only natural host.
  • 7. CLINICALFEATURES IP 15-45 days. Malaise, nausea, lassitude, myalgia, arthralgia and variable fever. Intestinal mucosa is in f lamed at this stage and loose stools are passed. Viruses excreted in stool and urine. Urine darkens as bilirubinuria increases and stools may be pale. Jaundice is f irst seen in sclerae and later skin. Fever resolves and virus excretion ceases as jaundice developed
  • 8. CLINICALFEATURES Patients are now no longer infectious and most feel better. After 7-10 days appetite returns and jaundice resolve No chronic or carrier stage. Complication is liver failure
  • 9. DIAGNOSIS Clinical suspcion Rule out other so send panel to con f irm Demonstration of speci f ic IgM by antibody capture EIA. Peak 2 weeks after elevation of liver negzymes and disappear within 3-6 months Ig G after Igm and persist for decades PCR HAV antigen detection
  • 10. PREVENTIONANDTREATMENT General hygiene No speci f ic antiviral treatement 2 vaccines 1. Formaldehyde inactivated vaccine 2. Live attenuated vaccine Also Human immunoglobulin for post exposure prophylaxis of intimate contacts
  • 12. INTRODUCTION Chronic infection with liver in f lammation leading eventually to cirrhosis and malignant change in liver. Vertical and horizontal infection from mother to child can produce successive generations pop chronically infected, infectious carriers
  • 13. VIROLOGYANDPATHOGENESIS Small enveloped virus containing partially ds DNA. 3 morphological forms- Spherical, tubular and Complete form. DNA contains 4 major genes that each encode more than one protein. Surface protein gene encodes 3 polypeptides including HBsAg make up the viral envelope C gene encodes core or capsid proteins and Precore protein. P gene encodes reverse transcriptase and RNAase and X gene encodes transactivator proteins. HBsAg is major protein of hep b virus. Major antigenic determinant is a antigen, antibodies to which confer protection after infection or vaccination.
  • 14. VIROLOGYANDPATHOGENESIS 2 pairs of mutually exclusive sub determinants- d or y, and w or r- giving 4 phenotypes add, add, aye and ayr. HBC Ag is major nucleocapsid antigen. HBeAg is cleavage product of HBcAg and is a marker in blood for HBV replication. Mutations in precore region of HBV causes faulty HBeAg. Around half of chronically infected HBsAg positive and HBeAg Nega posses this mutation.
  • 15. VIROLOGYANDPATHOGENESIS Mechanism of binding to cell not known. Most studies suggest virus not cytotoxic. 10% of patients persistent infection causes chronic hepatitis progressing to cirrhosis after 30 years. Persistent infection is thought to result from failure of initial immune response. Liver carcinoma 100 fold excess risk. Hep b gets incorporated into host chromosome but most of the viral genes are truncated
  • 16. EPIDEMIOLOGY Risk group 1. Iv drug users 2. Homosexual men 3. Sexual contacts of antigen positive persons 4. Residents in long stay homes for mentally handicapped people 5. Renal dialysis patients 6. Recipients of multiple blood products 7. Surgeons dentists 8. Infants of positive mothers
  • 17. EPIDEMIOLOGY Global HBV prevalence in HIV infected persons is 7.4% Presence of HIV greatly enhances risk of developing HBV associated cirrhosis and liver cancer
  • 18. CLINICALFEATURES IP 3-6 months. Upto 90% of cases are subclinical. Prodromal symptoms are followed by afebrile jaundice similar to that of HepA.. Prodrome Mild arthritis and faint rash. Clinically di ff icult to distinguish acute hepatitis. Patients with serum HBV DNA levels above 1000 are considered infectious why blood borne route. 5-10% patients become chronically infected. Leading to Cirrhosis and hepatocellular carcinoma.
  • 19. LABDIAGNOSIS • Antigen markers • HBsAg- First marker to appear • HBeAg- Indicates active viral replication and high infectivity • HBcAg- Not detected. Can be detected in hepatocytes • Antibody markers • AntiHBcAb- IgM indicates acute hepatitis and IgG appears in chronic hepatitis • AntiHBsAb marker o recovery or Vaccination • AntiHBeAb- indicates low viral replication and low infectivity. • Molecular markers. HBV DNA detection. Indicates active viral replication and high infectivity. Monitoring plays a load in treatment. • Non speci f ic markers- Liver enzymes
  • 21. TREATMENT Tenofovir and Telbivudine are the agent of choice Tenofovir and emtricitabine for HIV Other drugs lamivudine and peg interferon
  • 22. VACCINATIONS Active immunisations. Recombinant sub unit using surface antigen in bakers yeast by DNA recombinant technology Passive immunization - Hep b immunoglobulin