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39 Cards in this Set
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HAV
|
Hepatitis A Virus
a.k.a. "Infectious Hepatitis" When studying, think A for Acute, Age-related symptoms and Asymptomatic Infection (children) And, Antibody-detection (for diagnosis) |
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HAV
(epidemiology) |
World-wide distribution
Predominant in equatorial, developing countries MOST PREVENTABLE TRAVELER's DISEASE (vaccine) |
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HAV
(pathogenesis) |
Fecal-Oral Transmission (via food/water/contact)
1 month incubation period Virus shed in feces 2 weeks before symptoms |
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HAV
(Clinical Manifestations) |
VAST MAJORITY RESOLVE COMPLETELY
Children: Asymptomatic Symptoms of acute-infection increase with age |
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HAV
(Diagnosis) |
IgM Ab to HAV
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Hepatitis Viruses
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Little PHK-ERs (of Picorniviridae)
Tells you small, (+)ssRNA and naked |
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Hepeviridae
|
Family
Non-enveloped, ssRNA Gensus, Hepevirus |
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HEV
|
Hepevirus Genus, Hepeviridae Family (ssRNA, naked)
Major cause of sporadic/water-borne EPIDEMIC hepatitis Consider HEV w/returning travelers |
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HEV
(pathogenesis) |
Fecal-Oral Route
6 week incubation period ACUTE Self-Limited Hepatitis High Mortality during Pregnancy |
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HEV
(Diagnosis) |
IgM to HEV antigen
Rising IgG also diagnostic |
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HBV
|
Hepatitis B Virus
Of Hepadnaviridae (enveloped, dsDNA) |
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HBV
(Replication Anomaly) |
Even though dsDNA, first make RNA then reverse transcription to DNA
(weird RNA intermediate!) |
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Which Hepatitis Virus goes through an RNA intermediate during genome replication?
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HBV (of Hepadnaviridae)
|
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Hepadnaviridae
|
Family
As its name suggests, dsDNA (but with funky RNA intermediate and RT activity) |
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HBV
(Pathogenesis) |
Parenteral Inoculation
(makes sense, the thing is lipid-enveloped so you're not going to go through the GI tract) Incubation period is 3 months! Asymptomatic, persistant (children) to symptomatic acute hepatitis (healthy adults) |
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HBV DNA
|
Nucleic Acid of HBV
Best marker of active viral replication |
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Anti-HBs
|
Indications immunity to HBV acquired by infection or vaccination
|
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Antibody to what HB antigen is suggestive of IMMUNITY?
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Anti-HBs
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What Antibody is indicative of current/previous infection?
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Anti-HBc (the core antigen, of the nucleocapsid)
If IgM, current infection If IgG, previous infection |
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Possible outcomes of persistent (chronic) HBV
|
Chronic HBV (generally asymptomatic infection acquired in childhood)
May lead to chronic hepatits, cirrhosis or hepatocellular carcinoma (HCC) |
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HBV
(prevention) |
Recombinant HBV vaccine using HBV surface antigen
|
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HDV
(pathogenesis) |
Coinfection w/HBV
Superinfection in chronic HBV cases (acute/FULMINANT hepatitis, chronic liver disease) <- it's nasty |
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HDV
(general) |
Requires HBV
Delta antigen, encoded on ssRNA (circular) Enables RNA to get into nucleus & replicate |
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HDV
(outcome) |
If coinfection w/HBV, resolve
If superinfection, majority become chronic |
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HDV
(Diagnosis) |
Serology
Anti-HDV titers (IgM or rising IgG) and HDV antigen |
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HDV
(Vaccination) |
If HBV vaccinated, protected
If HBV (+), vaccine not available for protection against superinfection (they're screwed) |
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HCV
|
Of Flaviviridae (falvum = yellow . . . yellow fever, think blood. Also, think IV drug addicts and HepC. Tells you enveloped, (+) ssRNA
|
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HCV
(pathogenesis) |
Parenteral transmission (Pam An)
Acute, followed by persistent hepatitis MOST COMMON CAUSE OF CHRONIC HEPATITIS, possibly resulting in cirrhosis and liver failure |
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HCV
(Diagnosis) |
Antibody to HCV antigen
PCR can be used to monitor viremia and therapy |
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HCV
(Treatment) |
Ribavirin + interferon
Avoid EtOH and get vaccinated for HAV/HBV |
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HGV
|
Genus Flavirus
Of Flaviviridae (tells you enveloped, (+) ssRNA) NOT ASSOCIATED with Hepatitis but role in delaying AIDS! |
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Torque Tenovirus
|
Non-enveloped
Long-lasting viremia Correlation w/Hepatitis but role not proven |
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Prions
|
PRoteinaceous INfectious Particles
Abnormal PrP (precursor amyloid protein, of stem/neuronal cells) that catalyzes the conversion of normal protein to aberrant form. Abnl protein forms insoluble fibers and plaques |
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Prions
(Infection Control) |
Prions are resistant to head and most sterilization measures. Therefore, STRICT infection control is ABSOLUTELY NECESSARY
|
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Prions
(Pathogenesis) |
Acquired abnormal protein catalyzes the conversion of normal cell protein to aberrant form. Aberrant form accumulates, forms fibers and plaques - resulting in spongiform encephalopathies
|
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Prions
(Transmission?) |
May be transmissable (oral route, or transplants), idiopathic or inherited!
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Transmissable Spongiform Encephalopathies
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Oral/Transplant Transmission
Incubation period can be decades Absent immune response Rapidly progressive/fatal |
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Creutzfeldt-Jakob Disease
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Idiopathic Sponogiform Encephalopathy
~60 yeards w/rapid progression toward death (3-4 months) |
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Variant CJD
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Tranmissable Sponogiform Encephalopathy (BSE)
Mean age ~30 w/longer progression period Link to Mad Cow's Disease |