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Published byWinfred Thornton Modified over 9 years ago
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What is Hepatitis? General: inflammation of liver parenchyma cells
Worst case: life threatening liver cirrhosis, liver failure and/or liver cancer
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Normal Liver Balloon Degeneration
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Piecemeal Necrosis Cell Dropout
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Causes of hepatitis? Viral hepatitis
Primary: drug induced hepatitis, viral hepatitis Secondary: syphilis, T.B Viral hepatitis Hepatitis A virus (picornovirus) Hepatitis B virus (hepadnavirus) Hepatitis C virus (flavivirus) Hepatitis D, E, F, G viruses and non A-G Epstien-Barr virus Cytomegalovirus Yellow fever virus Infectious mononucleosis
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Hepatitis A Virus -HAV-
The Facts Picornaviridae, SSRNA, non enveloped Destroyed by autoclaving, boiling, dry heat Oral-fecal transmission Occurs as epidemic i.p 2-7 wks, mild jaundice, hepatospleenomegaly No carrier state Recovery within 2 months with solid immunity
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HAV viruses 27nm diameter
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Diagnosis and treatment
ELISA for HAV antibodies Treat complicated case with Ig. Prevention: decontaminate utensiles, cloths, water Vaccination to prevent spread of disease
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HEPATITIS B DNA and RNA (Hepadnaviruses) 3 forms of HBV in blood
small 22 nm (spherical 200 nm (filamentous) Dane particle 42 nm (spherical) infectious
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Viral antigens hepatocytes HBs Ag Abs are protective blood HBe Ag
Abs are not protective HBc Ag Abs not protective hepatocytes
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Infection varies Sub-clinical Fulminant (hepatic necrosis) Chronic carrier (hepatocellular carcinoma)
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Transmission Direct inoculation of blood or plasma (needle, transfusion) Indirect precutaneous (infected serum) skin cut, abrassion Adsorption of infected serum (mucosal surface) Adsorption of potentially infectious secretion (saliva, vaginal, semen) to mucosal surface oral-fecal …NO Role of saliva… Negative except human bite
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Incidence HBs is predominant in adults 21% oral surgeons
22% general surgeons 13-30 % dentists significant of HBs is carrier up to 10% in HBs infections
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Interpretation of serological markers
+HBs Ag: carrier and infectious persist for 6 months acute persist for year carrier Anti HBs : recovery and immunity vaccination HBe Ag: Acute disease of high infectivity if persist chronic liver damage Anti HBe: partial recovery from infection HBc Ag: present in liver Anti HBc: Active (recent infection)
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Typical Serological Courses of Infection
Symptoms HBeAg anti-HBe Total anti-HBc IgM anti-HBc anti-HBs HBsAg 4 8 12 16 20 24 28 32 36 52 100 Weeks after Exposure Tite Acute Hepatitis B Virus Infection with Recovery Typical Serological Courses of Infection HAV Infection Fecal HAV Symptoms 1 2 3 4 5 6 12 Total anti-HAV Tite ALT IgM anti-HAV Months after exposure IgM anti-HBc Total anti-HBc HBsAg Acute (6 months) HBeAg Chronic (Years) anti-HBe 4 12 24 36 52 Years Weeks after Exposure Titer Progression to Chronic HBV Infection 9
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Great risk to Dentist Known and unknown carriers
High risk patients include: Jaundice (6 months), Blood therapy (hemophilia and thalassemia), chronic renal failure, multiple blood transfusion, addicts and homosexual Prevention: Engerix B vaccine (subunit) 0, 1, 6, booster after one year
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HEPATITIS C RNA Chiron 1988 Transmition: post-transfusion, associated with hepatocellular carcinoma Diagnosis: ELISA for detection of Anti HCV Dental implication: lichen planus, oral malignancy, saliva contains HCV, Needle stick is common way of transmission
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HEPATITIS D Defective RNA requires HBs for function
Occurs as coinfection with HBV Transmitted parenterally Diagnosis by ELISA bad prognosis - higher incidence of liver necrosis, mortality
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HEPATITIS E RNA (Calicivirus) Transmission: fecal/oral
Disease: 3-6 week incubation, abrupt onset, mild except if pregnant, 20% fatality rate Jaundice: unknown Chronic: no
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1996, transmitted through blood cause mild disease, present in saliva
HEPATITIS F: post transfusion HEPATITIS G: 1996, transmitted through blood cause mild disease, present in saliva Transfusion transmitted virus(TTV) Post transfusional hepatitis, non envelop, ss RNA (parvo virus)
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