Hepatitis B/ Chronic Hepatitis/Serum Hepatitis
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Hepatitis B/ Chronic Hepatitis/Serum Hepatitis

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Hepatitis B/ Chronic Hepatitis/Serum Hepatitis Hepatitis B/ Chronic Hepatitis/Serum Hepatitis Presentation Transcript

  • • In the family Hepadnaviridae; common name: Hepadnavirus • Known as the smallest DNA virus • Double stranded, circular 42 nm DNA genome;Virion also called Dane particle • Normal virions consist of icosahedral nucleocapsid surrounded by a 27nm HBcAg and enveloped containing HBsAg (AKA enveloped Ag)-originally termed Australia Ag or Hepatitis asstd Ag (HAA).
  • 1. Infectious Hepatitis particles (Hepatitis B virion)- The virion has three forms of HBsAg (S,M,L) and nucleocapsid contains at least one HBcAg, polymerase protein, HBV genome 2. Non-Infectious Hepatitis particles i. Hepatitis B sphere- composed of the small and middle HBsAg ii. Hepatitis B filament-large HBsAg  Both particles have a diameter of 22nm and are composed solely of hepatitis B surface proteins. The absence of the hepatitis B core, polymerase, and genome reflects these particles' non-infectious nature
  • • Exposure to ether, acid (pH 2.4 for at least 6 h), and heat (98°C for 1 min; 60°C for 10 h) does not destroy immunogenicity or antigenicity; incomplete inactivation due to high [virus] • Antigenicity and probably infectivity are destroyed after exposure of HBsAg to 0.25% sodium hypochlorite for 3 min • Infectivity is lost after autoclaving at 121°C for 20 min or dry heat treatment at 160°C for 1 h
  • *HUMANS ARE RESERVOIR AND A VECTOR 1. BLOOD BORNE – BLOOD CONTAMINATED NEEDLES
  • – BLOOD CONTAMINTED OBJECTS
  • 2. SEXUAL-via oral, anal & vaginal – VAGINAL FLUID – SEMENAL FLUID 3. PRENATAL HIGH RISK INDIVIDUALS:  HEMOPHILIACS  DIALYSIS PATIENTS  IV DRUG ABUSERS  HEALTH CARE PERSONNEL  HOMOSEXUALLY ACTIVE MALES  HETEROSEXUALLY WITH MULTIPLE PARTNERS  INFANT OF INFECTED MOTHER
  • • Can enter into small tissue tears • Hepatitis B has a long incubation period of four weeks to six months during which time HBV infects the liver but is not cytolytic • Oncogenic-gene has a potential to cause cancer • Site of latency: Liver • Disease: – Acute infection with resolution (90%); – fulminant hepatitis most co-infected with delta virus (1%); – chronic hepatitis,persistence of HBSAg (9%) followed by resolution (disappearance of HBSAg),asymptomatic carrier state, chronic persistent (systemic disease without progressive liver disease),or chronic active disease (progressive liver damage
  • 1. Acute HBV infection is characterized by the presence of HBsAg and immunoglobulin M (IgM) antibody to the core antigen, HBcAg. During the initial phase of infection, patients are also seropositive for HBeAg(Antigenic determinant). 2. Chronic infection is characterized by the persistence (>6 months) of HBsAg (with or without concurrent HBeAg). Persistence of HBsAg is the principal marker of risk for developing chronic liver disease and hepatocellullar carcinoma (HCC) later in life. 3. The presence of HBeAg indicates that the blood and body fluids of the infected individual are highly contagious
  • Assay result HBsAg + AntiHBs - AntiHBc - Interpretation + +/- + - = + - - + Possibilities include: HBV infection in remote past; “lowlevel” HBV carrier; “window” between disappearance of HBsAg and appearance of Anti-HBs; or false+ or nonspecific reaction. Investigate with IgM anti-HBc. When present, AntiHBe helps validate the Anti-HBc reactivity - - - Never infected with HBV. Possibilities include another infectious agent, toxic injury to liver etc. - + - Vaccine-type response Early acute HBV infection. HBV infection either acute or chronic. Differentiate with IgM Anti-HBc. Determine level of replicative activity (infectivity) with HBeAg or HBV DNA Indicates previous HBV infection and immunity to Hepatitis B
  • • Diagnosis: Serology, viral antigen detection and PCR • Treatment: Antivirals and liver transplant for fulminant disease • Prevention: – HBV vaccine; hepatitis B immune globulin