What is Hepatitis? General: inflammation of liver parenchyma cells Worst case: life threatening liver cirrhosis, liver failure and/or liver cancer

Normal Liver Balloon Degeneration

Piecemeal Necrosis Cell Dropout

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

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

HAV viruses 27nm diameter

Diagnosis and treatment ELISA for HAV antibodies Treat complicated case with Ig. Prevention: decontaminate utensiles, cloths, water Vaccination to prevent spread of disease

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

Viral antigens hepatocytes HBs Ag Abs are protective blood HBe Ag Abs are not protective HBc Ag Abs not protective hepatocytes

Infection varies Sub-clinical Fulminant (hepatic necrosis) Chronic carrier (hepatocellular carcinoma)

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

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

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)

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

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

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

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

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

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)