Viral hepatitis BY Akash Sengupta (2nd year medical student)

on

  • 279 views

it is a point-wise representation of viral hepatitis. this is mainly concerned with the pathogenesis rather than the morphology of the diseases for which last few slides have been left blank. this ...

it is a point-wise representation of viral hepatitis. this is mainly concerned with the pathogenesis rather than the morphology of the diseases for which last few slides have been left blank. this will help in rapidly recapitulating what you've read about the topic in the past and assort it in a orderly manner. hope some will find it helpful.

Statistics

Views

Total Views
279
Views on SlideShare
279
Embed Views
0

Actions

Likes
0
Downloads
5
Comments
0

0 Embeds 0

No embeds

Accessibility

Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Processing…
Post Comment
Edit your comment

Viral hepatitis BY Akash Sengupta (2nd year medical student) Viral hepatitis BY Akash Sengupta (2nd year medical student) Presentation Transcript

  • 1. It is a „picornavirus‟ of „heparovirus‟ genus; 2. Capsid is 27 nm in diameter; eicosahedral; 3. Got single stranded RNA;
  • 1. self-limited disease; 2. Rarely causes fulminant hepatitis; 3. Does not cause carrier state or chronic hepatitis; 4. Becomes significant only when superimposed over chronic hepatitis due to hepatitis B/C virus or alcohol; 5. The disease usually develops in children and rare in adults; it is endemic in areas and happens all over the world; 6. Within 10 years most people in developed country develop seropositivity; 7. It is usually a sporadic febrile illness; 8. Accounts for 25% of total hepatitis cases; 9. Incubation period is 2-6 weeks;
  • 1. Spread by ingestion of contaminated food and water; 2. Shed in stool 2-3 weeks before and 1 week after the onset of jaundice; 3. Infection spreads to other persons during this period by foeco-oral route; 4. School, hospital outbreaks are more common; over-crowding and bad sanitary system predispose to the disease; 5. People taking poorly cooked sea-shells, oysters, mussels, clams are susceptible as these organisms concentrate this virus from human sewage contaminating the sea-water; 6. Infected food-handlers are also source of infection; 7. Consumption of raw vegetable can be a cause; 8. Not significantly shed in tear, saliva or semen; 9. As Hepatitis A viremia is transient there is less chance of blood-borne disease and hence blood to be transfused is not screened for this virus;
  • 1. IgM appears at the onset of symptoms; 2. Its titre rises as the fecal shedding declines; 3. IgM titre declines after a few months; 4. IgG titre rises with its fall; 5. IgG provides protective immunity against HAV for rest of the life;
  • 1. HepaDNAviridiae 2. Spherical; diameter 42 nm; “dane” particle; 3. Inside electron-dense; 28 nm; 4. Partially double-stranded DNA with 3200 nucleotides each coding for proteins; 5. HBcAg or „core‟ protein remains in the blood for assembly of complete virion; 6. HBeAg or „envelope‟ protein directs towards secretion (pre-core) or signifies ongoing infection (core); 7. HBsAg or „surface‟ protein synthesized and secreted by infected hepatocytes as 22 nm spheres and tubules; 8. DNA polymerase with reverse transcriptase activity is present; 9. HBxAg or antigen coded from the X region is necessary for viral replication; acts as a transcriptional transactivator; may contribute to formation of hepatocellular carcinoma by dysregulating the cell cycle control (activation of proto-oncogenes)
  • 1. It may produce- a. acute hepatitis with resolution; b. chronic hepatitis that leads to cirrhosis; c. fulminant hepatitis leading to massive hepatocellular necrosis; d. back-drop for hepatitis D infection; 2. It also plays important role in development of hepatocellular carcinoma; 3. Incubation period is 4-26 weeks; 4. Found in blood up to and during acute and chronic hepatitis; 5. Found in tear, saliva, semen, breast milk and all other pathologic body fluids; 6. NOT FOUND IN STOOL UNLIKE HAV; 7. Vehicles of transport are saliva, tear, vaginal secretion, blood, breast milk, exudate, transudate etc; Transmission is through unscreened blood transfusion, IV drug abuse, needle stick injury, vaginal secretion, homosexual practices, dialysis etc; importantly, vertical transmission occurs from infected pregnant mother to her child through placental barrier; 8. The virus is highly resistant to heat and humidity; 9. One third cases are due to unknown causes; 10. IgG anti-HBV virus gives protection against infection, hepatocellular malignancy;
  • 1. Mainly two phases-(a) integrative phase; (b) proliferative phase; 2. In integrative phase the viral DNA is incorporated into the host DNA but no symptoms appear; 3. In proliferative phase, viral DNA is in “Episome” form and there is synthesis of all the viral proteins including HBc, HBs, HBe, HBs , HBx etc; 4. In proliferative phase this viral peptides are presented along with MHC I gene on the infected hepatocytes; specially HBsAg and HBcAg; 5. CD8+ cells recognize these and kills the infected hepatocytes; 6. There is massive liver necrosis; 7. With the appearance of antibody the viral replication halts and the liver damage subsides but the chance of hepatocellular carcinoma still remains; 8. CD8+ cells cause liver injury, remove the infected cells and there is a role of γ- interferon; 9. People with immuno-suppression has less severe liver damage and has greater possibility to emerge as carriers; 10. Antibody response develops after the cellular response but is effective in preventing the farther progression of the disease;
  • 1. Incubation period 4-26 weeks; 2. HBsAg rises just before the onset of the symptoms; it peaks at overt diseases and declines under detectable level over 3-6 months; 3. HBeAg, HBV-DNA, DNA polymerase follow rise in HBsAg; these are indicative of active viral replication; 4. Anti-HBc IgM level rises just before the onset of the symptoms, concurrently with serum amino-tranferase; 5. Over time, anti-HBc IgM is replaced by anti-HBc IgG; 6. Anti-HBe IgM develops just after disappearance of HBeAg from blood; indicates peaking of acute disease and that the disease is on wane; 7. Anti-HBs IgG develops only after the acute disease is over; it may remain undetected for weeks to months; 8. This remains in blood till death and provide protective immunity; so non-infective HBsAg is used now as passive vaccine; 9. If blood level of HBsAg remains elevated asymptomatically for more than 6 months, the patient is said to develop a carrier state; 10. Chronic replication of HBV virions lead to persistence of HBsAg, HBeAg, HBV- DNA usually with anti-HBc antibody or occasionally anti-HBs antibody;
  • 1. Hepacivirus occupying a genus in flaviviridae; 2. Small, enveloped, single stranded RNA containing virus; 3. A 9kb genome encodes a single polyprotein from which functional components are cleaved; 4. 340 nucleotides in the 5‟ end and 128 nucleotides in 3‟ end are not translated; binds viral proteins and plays significant role in viral replication and maintenance of genome stability; 5. Encoded structural proteins are- a highly conserved nucleotide core protein, two envelop proteins E1 and E2 among which E2 has got two hypervariable regions HVR1 and 2; 6. Non-structural proteins are P7 (probably a metallo-protease), NS2, NS3, NS4a/4b, NS5a/5b; 7. The last one is the viral RNA dependant RNA polymerase; 8. Towards the 3‟ end the sequence are less conserved and subject to constant change; 9. NS5b has poor fidelity and hence there happen constant mutations viral antigens over replications leaving the antibodies ineffective; 10. In a patient who has been infected by a strain of HCV, a number of different strains are found which have been derived from the original infecting virus through mutations. To be continued…..
  • 1. E1 protein (envelope) is target to many antibodies; but it is the most variable protein and thus emerging virus escapes neutralization by antibody; 2. Elevated titre of anti-HCV IgG does not confer immunity, nor does the vaccine for the same reason; 3. NS5a and E2 inhibit interferon-induced double-stranded RNA-activated protein kinase and thus escapes interferon mediated cell damage; 4. So massive hepatic damage seen in HBV infection is absent here; 5. HCV infection is characterized by repeated bouts of hepatic injury due to reactivation of pre-existing infection or emergence of a new mutated strain; 6. Chronic persistent infection is hallmark of this disease; 7. After 5-20 years, cirrhosis develops;
  • 1. Incubation period is 2-26 weeks; 2. Disease is usually asymptomatic as the liver injury is not significant; 3. In most cases the infection results from inoculation, blood transfusion, IV drug abuse, among health personnel, unprotected sex and haemodialysis; 4. Vertical transmission is less common than in HBV infection; 5. The group most susceptible is IV drug abusers; other groups are homosexuals, house carriers, haemodialysis patients and haemophiliacs; 6. Patients with unexplained liver cirrhosis and HCC have seropositivity for HCV in more than 50% cases; 7. Acute infection is asymptomatic and undetectable; 8. Majority of infected persons gradually progress to chronic liver disease specially liver cirrhosis(20% cases);
  • 1. HCV-RNA is present in the blood for 1-3 weeks; coincident with elevation of serum transaminase; 2. In 50-70% cases anti-HCV antibodies are detected; in the rest, it appears after 3-6 weeks; 3. The course of disease is less aggressive than HBV; 4. In chronic hepatitis patients HCV-RNA persists in the blood in spite of presence of neutralizing antibody; 5. So, screening for HCV-RNA should be done in people with chronic hepatitis to assess viral replication and confirm HCV infection; 6. A quite characteristic clinical feature of HCV infection is episodic rise in serum transaminase intervened by normal serum level;
  • 1. 35 nm double-shelled particle that on electron microscopy resembles the “dane”- particle appearance of HBV; 2. HBsAg surrounds an internal polypeptide assembly called HDAg ; 3. It has in its core a circular single stranded RNA having the shortest length among any animal genome; 4. HDAg is the only product of the genome detected till date; 1. It is unique in that it can replicate only when encapsulated by HBsAg; 2. So either co-infection with HBV or superinfection in chronic/carrier HBV infected patients; 3. Three courses may be taken by the disease- (a) an acute severe hepatitis may erupt in a patient who was previously healthy; (b) mild HBV hepatitis may be converted to fulminant hepatitis; (c) chronic, progressive disease develops (most cases), often culminating in cirrhosis; 4. In Africa, Middle East and southern Italy, 20-40% HBV carriers show HDAg positivity; but in USA this is not the same and the disease is mainly seen in drug addicts and haemophiliacs (1-10%);
  • 1. HDV RNA is detected in blood and liver prior to and during early days of acute infection; 2. IgM anti-HDV is the most reliable marker of recent infection but its appearance is late and transient; 3. IgM against both HDAg and HBcAg is the best indicator of acute co-infection; 4. Presence of HBsAg in the serum and persistence of IgM-anti-HDV for weeks to months is the best indicator of superimposed HDV infection on chronic HBV infection;
  • 1. Un-enveloped single stranded RNA virus with 7.6 kb genome resembling Calciviridae; 2. Viral particles are 32-34 nm; 3. HEV antigen found in cytoplasm of hepatocytes during acute infection and virions are shed in stool; 1. Incubation period 6 weeks; 2. Enterically transmitted water-borne infection; 3. Disease more common in young to middle aged adults ; sporadic infection in children is uncommon; 4. Epidemics reported from Asia, Indian subcontinent, Mexico and sub-Saharan Africa; 5. HEV infection accounts for >50% cases of sporadic acute hepatitis exceeding the number of cases byHAV infection; 6. HEV infected pregnant women have high mortality rate approaching 20%; 7. Never shows chronic manifestation or persistent viremia;
  • 1. Before onset of acute disease, HEV RNA and HEV virions are present in liver and stool; 2. Rise in serum aminotransferase, clinical illness and raised anti –HEV IgM are virtually simultaneous; 3. Symptoms resolve in 2-4 weeks; 4. During this period IgM is gradually replaced by IgG which is persistently present is serum thereafter providing immunity;
  • 1. Hepatitis G virus resembles hepatitis C virus (flavivirus); 2. Hepatitis GB virus type C is transmitted through blood or sexual contact; 3. Seen in dialysis patients and In 25% cases HGV infection may become chronic; 4. This virus usually replicates in the mononuclear cells and as such it is not a hepatoivrus; 5. It doesn‟t elevate serum aminotransferase level; 6. Usually co-infects patients with HIV infection and this combined infection is protective against HIV disease; 1. Acute asymptomatic infection with remission; 2. Acute symptomatic infection with remission; 3. Chronic hepatitis with or without progression to liver cirrhosis; 4. Fulminant hepatitis with massive to submassive hepatic necrosis;