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Hugh B. Fackrell Filename: Hepatite.ppt
Viral Hepatitis Hugh B. Fackrell Filename: Hepatite.ppt
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Hepatitis Virus Outline
Definitions Classification Structure Multiplication Clinical manifestations Epidemiology Diagnosis Control Baron’s Web Site
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Hepatitis an ancient disease, the etiology has only recently (50 yrs.) been revealed.
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Hepatitis An inflammatory disease
necrosis of hepatocytes mononuclear response destroys liver architecture Liver excretion of bile pigments such as bilirubin into the intestine is interrupted
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Bilirubin Bilirubin: greenish-yellow pigment accumulates in the blood and tissues Jaundice - yellow tinge in the skin and eyes caused by bilirubin
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Types of Jaundice Pre hepatic: Hemolytic Jaundice
normal feces, anemia, reticulocytes Hepatic: Hepatocellular Jaundice fecal fat, bilirubinuria, Alkaline phosphatase high, gamma globulins high Post Hepatic: Obstructive Jaundice fecal fat, bilirubinuria, alkaline phosphatase high
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Jaundice of the Newborn
Premature infants bilirubin increases from birth peaks at one week caused by 1:excessive hemolysis 2:immature liver function
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Hepatitis symptoms Swelling and tenderness of liver
Jaundice -yellow tinge in the skin and eyes dark urine transaminase, alkaline phosphatase levels increased
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Viral Hepatitis Liver infection caused by several UNRELATED VIRUSES
Inflammation and necrosis of the liver 50% of HAV & HBV are subclincal
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Hepatitis types Hepatitis A - HAV "infectious hepatitis"
Hepatitis B - HBV "serum hepatitis" Hepatitis C - HCV non A, non B Hepatitis D - HDV Delta virus Hepatitis E - HEV similar to type “A”
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“Infectious hepatitis” “Epidemic hepatitis” HAV
Hepatitis A “Infectious hepatitis” “Epidemic hepatitis” HAV
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Hepatitis A Clinical manifestations
asymptotic or anicteric in children 3-5 week incubation period liver inflammation malaise - flu like symptoms self limiting low mortality
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Hepatitis A Structure Picornavirus Only one serotype
Enterovirus type 72 27-29 nm icosahedral ssRNA
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Hepatitis A Host Defenses
antibodies develop late in incubation period IgM within a week of dark urine peaks a week later lasts days IgG after IgM peaks days lasts many years
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Hepatitis A Epidemiology
Global distribution- underreported Fecal-oral route, person to person water Overcrowding & poor sanitation Infected food handlers common vector
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Annual Incidence Viral food borne diseases
Total Viral food borne 30,883,391 Total Microbial food borne incidence 38,629,64 Norwalk-like viruses 23,000,000 Rotavirus 3,900,000 Astrovirus Hepatitis A 83,391 Food-Related Illness and Death in the United Stateshttp:// CDC
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Hepatitis A Diagnosis Clinical manifestions Viral antigens
Immunoelectron microscopy RIA ELISA Immune Adherence hemagglutination (old method) Viral antibodies
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Hepatitis A Control No specific control Improve hygiene and sanitation
Human immunoglobulin 2 IU anti Hepatitis A /kg body weight HAV vaccines in clinical field trials
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Hepatitis B “Serum hepatitis” HBV
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Hepatitis B Clinical Manifestations
typical viral hepatitis symptoms 4-26 week incubation period more severe than HAV CHRONIC PERSISTENT HEPATITIS CHRONIC ACTIVE HEPATITIS
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Hepatitis B Structure Hepadnavirus dsDNA, circular, 3200 nucleotides
enveloped icosahedral virus 42 nm
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Australia antigen “Dane particle”
small pelomorphic particles 20-22nm tubular forms excess viral capsids released into blood stream
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3 forms of HBV
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Dane Particles
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Hepatitis B Host Defenses
Cell mediated Immunity important for recover in acute phase autoimmune liver damage in chronic infections Humoral Immunity not always protective HBsAg for Vaccines Interferon not detected during infection exogenous application effective
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Hepatitis B Epidemiology
Parenterally ie via blood, saliva, menstrual and vaginal discharges, semen and breast milk infected blood and blood products sexual contact perinatally from mother to child
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Hepatitis B Prevalence
AREA HBsAg anti HBsAg Western Europe % % USA Eastern Europe % % USSR China % % Asia
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Hepatitis B Diagnosis Electron microscopy Viral DNA polymerase
Viral DNA probes Serology
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Corresponding antibodies to each antigen occur
Hepatitis B Serology Hepatitis B surface antigen- HBsAg 10 subtypes Hepatitis B core antigen- HBsCAg Soluble core associated antigen HBeAg Corresponding antibodies to each antigen occur
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Hepatitis B Control No specific control Passive Immunization
HBV immunoglobulin IU within 48 hours neonates of infected mothers -immediately after birth Active Immunization HBsAg recombinant DNA in yeast
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HBV & Cancer 1. Transformation of the cell by virus
2. Helper virus if the transforming virus is defective 3. Co-carcinogen, chemical, cigarette smoke
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Transformed cells lose contact inhibition continue to divide
form random aggregations can become invasive Not warts: Papovavirus
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Primary Hepatocellular Carcinoma
Highest incidence: Central Africa Southeast China Pacific Islands, Borneo, Sarawak, Taiwan Icteric symptoms: jaundice, dark urine, pale stools Global ,000- 1,000,000 deaths /year U.S.A deaths / year
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Acute HBV & Cancer Acute Hepatitis B
90% 1% Resolution Fulminant Hepatitis 50% Resolution Chronic Active Asymptomatic Carrier Hepatitis Chronic Cirrhosis Hepatic Cell Carcinoma Extrahepatic Disease
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Hepatitis C HCV Non -A Non-B
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Hepatitis C Clinical Manifestations
resembles HBV persistent carrier state 50% of patients have chronic liver damage associated with hepatocellular carcinoma
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Hepatitis C is probably caused by several different viruses
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Hepatitis C Epidemiology
in USA causes 90% of post transfusion hepatitis Mother to infant transmission
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Hepatitis C Diagnosis C100-3 recombinant viral antigen
anti c100-3 marker of chronic infection
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Hepatitis A HAV Hepatitis B HBV Hepatitis C HCV Structure
Cultured in cells Epidemiology Transmission Incubation period Symptoms Jaundice Onset Vaccine Diagnostic tests RNA yes endemic & epidemic oral/fecal, water & food weeks fever, G-I tract disorder 1 case in 10 acute/short not available DNA no endemic blood/serum, close contact 1-6 months fever, rash, arthritis common gradual/chronic yes HBV no endemic blood/serum, intimate contact 2-8 weeks similar to HBV common acute/chronic not available yes
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Hepatitis D HDV
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Hepatitis D Dependovirus, it is defective and cannot produce infection unless the cell is also infected with HBV. Viroid - a naked strand of RNA that enters the cell in piggy-back fashion.
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Hepatitis D Clinical Manifestations
Dual infection is more severe than HBV fulminating hepatitis severe rapidly progressive hepatitis severe exacerbations
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Hepatitis D Structure 35-37 nm virus particle
shares coat protein of HBV small RNA genome one serotype
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Hepatitis D Epidemiology
hemophiliacs and IV drug users Contaminated blood and blood products
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Geographic distribution of HDV
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Hepatitis D Diagnosis Clinical manifestations Delta antigen
Immunofluorescence RIA ELISA Anti delta antigen same as above
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Hepatitis E Virus
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Hepatitis E fecal/oral route
predominantly found in developing countries but is world wide. symptoms similar to HAV but mortality 1-2% (ten times that of Hepatitis A). epidemics - India, Pakistan, Nepal, Burma, North Africa and Mexico.
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