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Kerriann Parchment GI CBL 2 Part 3 December 2012 Viral hepatitis serology.

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Presentation on theme: "Kerriann Parchment GI CBL 2 Part 3 December 2012 Viral hepatitis serology."— Presentation transcript:

1 Kerriann Parchment GI CBL 2 Part 3 December 2012 Viral hepatitis serology

2 Hepatitis A ssRNA virus Transmitted via Fecal-Oral route Outbreaks are associated with Children in daycare Men who have sex with men IVDU International travelers Contaminated seafood Usually causes self-limiting acute illness Does not cause chronic hepatitis Rarely causes fulminant hepatitis No carrier state

3 HAV Serology Anti-HAV IgM’s are present at the onset of symptoms and make a reliable marker of acute infection Remains for 4-6 months Anti-HAV IgG’s Titers rise when anti-HAV IgM’s decline Confer long-term immunity

4 Hepatitis B DNA virus Transmitted via parental, sexual fluids, perinatal Perinatal transmission is the main means of transmission in high prevalence areas Unprotected sex and IVDU are main means of transmission in low prevalence areas such as the U.S. Causes: Acute hepatitis with complete clearance Chronic hepatitis Non-progressive Progessive resulting in cirrhosis Fulminant hepatitis with massive necrosis Inactive Carrier state

5 HBV serology HBV DNA Present when there is active or chronic disease Inactive carriers or those immunized don’t have HBV DNA Antigens HbsAg- surface antigen that is present during active disease (acute or chronic) HbcAg- protein present in the core and is not detectable in serum HbeAg- secretory protein and is marker of replication Antibodies Anti-Hbs- neutralizes HbsAg and its presence indicates resolved infection Anti-HbcIgM- marks acute infection and period during window period (period between disappearance of HbsAg and anti-Hbs) Anti-Hbc IgG- can appear in acute resolved infection or chronic HBV Anti-HbeAg- seroconversion occurs early in acute infections and can occur later in chronic infections

6 HBV serology Acute HBV (unresolved) HbsAg Anti-HBc IgM HbeAg High levels of HBV DNA Acute HBV window period Anti-Hbc IgM Low levels HBV DNA Resolved HBV infection Anti-Hbc IgG Anti-Hbs Chronic HBV HbsAg Anti-Hbc IgG Low levels of HBV DNA Inactive chronic carrier state HbsAg Anti-Hbc IgG Anti-HBe

7 Hepatitis D Defective RNA virus that co-infects with HBV Requires HBV to complete virion assembly and secretion HDV can replicate on its own Acute infections: anti-HDV IgM Chronic infection: anti-HDV IgG

8 HCV Compared to HBV, more cases progress to chronic infection or cirrhosis It is the leading cause of cirrhosis in the U.S. Transmitted via IVDU Intranasal drug use Blood products Occupational risks tattoos

9 HCV serology Acute HCV: HCV RNA can be detected by PCR Infection will be cleared with development of Anti-HCV antibodies Spontaneous clearance can occur in 14% of HCV patients

10 HEV Single stranded RNA virus Fecal oral transmission Disease is most common in adult between the ages 15-40 Causes self limiting disease in adults and there is no chronic state However, in pregnant women, the disease is more severe and can cause fulminant hepatic failure Anti-HEV Igm- Arise with the onset of symptoms Anti-HEV IgG- will develop after symptoms resolve (2-4 weeks)

11 Works Cited Dr. Dubrovskaya. Lecture 14: Viral Hepatitis Robbins and Cotran Chapter 18: Liver and Biliary Tract

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