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GI Week 5 - WLB > Viral Hepatitis - Diebel > Flashcards

Viral Hepatitis - Diebel Flashcards

1
Q

What two viral hepatitis infections cause acute only infections and lead to lifelong immunity after infection recovery with no risk of Hepatocellular Carcinoma?

A

Hepatitis A Virus

and

Hepatitis E Virus

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2
Q

What three viral hepatitis infections cause acute and chronic infections?

A
  1. Hepatitis B Virus
  2. Hepatitis C Virus
  3. Hepatitis D Virus
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3
Q

Hepatitis A Virus (HAV) classification:

DNA/RNA

Nucleocapsid Shape

Envelope Yes/No

Genome

Family

Genus

A
  • RNA virus
  • Icosahedral Nucleocapsid
  • Nonenveloped
  • SS (+) Nonsegmented Genome (Class IV)
  • Picornaviridae
  • Enterovirus
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4
Q

Why does HAV not get destroyed in the gut?

A

The capsid structure is one of the most stable of all picornaviruses and is stable at pH 1, resistant to destruction by many solvents and detergents and desiccation.

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5
Q

How is HAV transmitted?

A
  • Fecal-to-oral route
    • Contaminated seafood - Shellfish
    • Imported berries
    • Travelers
    • Day care, summer camps, schools
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6
Q

What is the HAV route of infection?

A
  • fecal to oral
    • mouth → gut → blood → liver → blood
  • Infects cells expressing the HAV cell receptor 1 glycoprotein (HAVCR-1).
  • Found on liver cells and T cells
  • Virus replicates in large quantities in the liver
    • virus shed in the stool approximately 10 days before the onset of jaundice.
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7
Q

What leads to the pathogenesis and disease associated with Hepatitis A viral infection?

A
  • The immune response to virally infected liver cells, mediated by cytotoxic T cells, leads to the pathogenesis and disease associated with this infection.
  • HAV it self is not cytotoxic.
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8
Q

Approximately 40% of acute cases of hepatitis are caused by what virus?

A

Hepatitis A virus

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9
Q

What is the incubation period for HAV? When is it contagious?

A
  • Incubation = short (weeks)
  • Virus spreads readily in the population because most people are contagious 10 -14 days prior to the onset of symptoms.
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10
Q

What is the clinical course for HAV infection?

A
  • Asymptomatic (usually)
  • 90% of all children and 25-50% of infected adults have asymptomatic, productive infections.
  • Acute infection:
    • Symptoms occur 15-50 days post-exposure and intensify for 4-6 days.
      • Fever, fatigue, nausea, loss of appetite, abdominal pain, dark urine, jaundice
    • Complete recovery 99% of the time.
    • Occasionally HAV causes a fulminant infection which is associated with an 80% mortality rate.
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11
Q

What laboratory test is used to diagnose HAV infection?

A
  • Acute infection shown by ELISA of anti-HAV IgM
    • best test to detect acute hepatitis A
  • Prior HAV infection and/or prior vaccination shown by detection of anti-HAV IgG
    • protects against reinfection
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12
Q

What is seen on liver biopsy in HAV infection?

A
  • Hepatocyte swelling
  • Monocyte infiltration
  • Councilman bodies
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13
Q

What is the treatment for HAV infection?

A
  • Supportive care → self-limiting infection
  • Pooled immune globulins
    • only effective if given early in the incubation period (<2wks after exposure)
  • Prophylaxis with immune globulin serum.
    • Given to contacts of a HAV infected individual.
  • Killed HAV vaccine.
    • Routine HepA vaccine.
      • 2 dose vaccine series started between 12 and 23 months of age.
      • Separate the 2 doses by 6 to 18 months.
  • Catch-up vaccination (any person above the age of 2). 2 doses of the HepA vaccine separated by 6 to 18 months.
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14
Q

How can HAV spread be controlled?

A
  • good hygiene
  • HAV passive antibody protection for contacts
  • HAV vaccine.
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15
Q

Hepatitis E Virus (HEV) classification:

DNA/RNA

Nucleocapsid Shape

Envelope Yes/No

Genome

Family

Genus

A
  • RNA virus
  • Icosahedral Nucleocapsid
  • Nonenveloped
  • SS (+) Nonsegmented Genome (Class IV)
  • Caliciviridae
  • Calicivirus
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16
Q

What is the HEV route of infection?

A
  • Fecal-to-oral
    • fecal to oral
      • mouth → gut → blood → liver → blood
  • Found on liver cells and T cells
  • Virus replicates in large quantities in the liver
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17
Q

How is HEV transmitted?

A
  • Fecal-to-oral route
    • Contaminated water
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18
Q

What is the incubation period for HEV?

A

Short (weeks)

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19
Q

What is the clinical course for HEV infection?

A
  • Symptoms of disease occur slightly later than seen with HAV
  • Disease is slightly more severe with an overall mortality rate of around 1 to 2%
  • Fulminant hepatitis in Expectant (pregnant) women
    • mortality rate of ~20%
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20
Q

What is HEV infections so dangerous in pregnant women?

A
  • Immunological and hormonal factors
    • In pregnant women the maternal immune system is altered.
    • T cells are reduced up to the 20th week of gestation → speculated to lead to an increased susceptibility to viral infections such as hepatitis, rubella, herpes, and HPV.
    • Levels of HCG → suppressive effect on cell-mediated immunity.
  • Liver damage is still through immunological mediated injury . . . ?
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21
Q

What is the global distribution of HEV infection?

A
  • HEV may be responsible for 2/3 of epidemic “non-A and non-B” hepatitis cases in:
    • India
    • Russia
    • China
    • North Africa
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22
Q

What laboratory test is used to diagnose HEV infection?

A

Presence of anti-HEV antibody or HEV RNA (PCR).

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23
Q

What is the treatment for HEV?

A
  • None available
  • Immunoglobulin serum can be given to exposed individuals.
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24
Q

Who is most at risk for developing HAV and HEV infection?

A
  • Risk factors can include overcrowded, unsanitary cities.
  • People at risk include:
    • Children – mild disease, major source of the spread of HAV
    • Adults – abrupt-onset hepatitis
    • Pregnant women – high mortality rate with HEV infections
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25
Q

Hepatitis B Virus (HBV) classification:

DNA/RNA

Nucleocapsid Shape

Envelope Yes/No

Genome

Family

Genus

A
  • DNA virus
  • Icosahedral Nucleocapsid
  • Enveloped
  • DS (partial) Circular DNA (Group VII)
  • Hepadnaviridae
  • Orthohepadnavirus
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26
Q

What part of the Hepatitis B virus is infectious?

A
  • The infectious virion itself is the “Dane” particle.
  • Others are HBsAg only particles, no core.
    • Not infectious.
    • Throws off the immune system?
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27
Q

How is HBV transmitted?

A
  • Parenteral → Blood
  • Sexual → Baby-making
    • multiple sexual partners
    • unprotected intercourse
  • Perinatal → Birthing
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28
Q

What is the incubation period of HBV?

A

Long → months

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29
Q

What is the route of infection of HBV?

A
  • Bloodborne pathogen
  • Infects liver cells expressing:
    • transferrin receptor
    • asialoglycoprotein receptor
    • human liver annexin V protein
  • Infects cells by using the HBV HBsAg viral protein
  • The major source of infectious virus is in the blood but it can also be found in semen, saliva, milk, vaginal and menstrual secretions, and amniotic fluid.
  • Virus starts to replicate win the liver within 3 days of exposure.
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30
Q

What is the clinical presentation of HBV infection?

A
  • Acute → jaundice, fever, arthralgias
    • Immune complexes formed between HBsAg and anti-HBs contribute to hypersensitivity reactions (Type III) leading to vasculitis, rash, etc.
  • Chronic infection → carrier state, asymptomatic, or slowly progressing disease leading to cirrhosis
    • can exhaust CD8 T cells preventing them from killing cells.
      • Late in infection there are also large amounts of HBs in the serum which binds to and blocks neutralizing Ab that would normally attack the infectious virus particles.
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31
Q

What is the clinical course of HBV infection?

A
  • Symptoms of infection may take up to 45 days after transmission.
  • Virus causes acute or chronic, symptomatic or asymptomatic diseases.
  • Initially like serum sickness
    • fever, arthralgias, rash
    • may progress to carcinoma (HCC)
  • The individual’s immune response to the initial infection dictates the outcome of the disease.
    • strong response → severe course that resolves quickly
    • weak response → mild but chronic course
32
Q

How is HBV infection diagnosed?

A
  • Patient Hx
  • Presence of liver enzymes → elevated ALT/AST
  • Serology
    • HBsAg
    • Anti-HBs
    • HBcAg
    • Anti-HBc
    • HBeAg
    • Anti-HBe
33
Q

What is HBsAg?

A
  • HBV surface antigen
  • Indicates HBV infection
  • Present months 1-5
34
Q

What is Anti-HBs?

A
  • Antibody to HBsAg
  • Presence of antibodies against HBsAg signals protection / neutralization.
    • Indicates immunity to Hepatitis B
  • Present months 6+
35
Q

What is HBcAg?

A
  • Core antigen
36
Q

What is Anti-HBc?

A
  • Antibody to HBcAg
    • IgM = acute/recent infection
      • may be the sole positive marker of infection during window period
    • IgG = prior exposure or chronic infection
  • Present months 2-8+
37
Q

What is HBeAg?

A
  • Antigen secreted by infected hepatocyte into circulation
  • Not part of mature HBV virion
  • Indicates active viral replication → high transmissibility
    • ​present months 2-4 during prodrome, acute disease, and symptomatic stage
38
Q

What is Anti-HBe?

A
  • Antibody to HBeAg
  • Indicates low transmissibility
    • marker for treatment effectiveness
39
Q

What hepatitis serologic markers would be present during Acute HBV?

A
  • HBsAg
  • HBeAg
  • Anti-HBc IgM
40
Q

What hepatitis serologic markers would be present during the window period of HBV?

A
  • Anti-HBe
  • Anti-HBc IgM
41
Q

What hepatitis serologic markers would be present during Chronic HBV with high infectivity?

A
  • HBsAg
  • HBeAg
  • Anti-HBc IgG
42
Q

What hepatitis serologic markers would be present during Chronic HBV with low infectivity?

A
  • HBsAg
  • Anti-HBe
  • Anti-HBc IgG
43
Q

What hepatitis serologic markers would be present during Recovery of HBV?

A
  • Anti-HBs
  • Anti-HBe
  • Anti-HBc IgG
44
Q

What hepatitis serologic markers would be present in a patient immunized against HBV?

A
  • Anti-HBs
45
Q

What is the treatment for HBV infection?

A
  • Prophylaxis with immune globulin serum contains anti-HBsAg antibodies
    • Given to newborns of HBsAg-positive mothers to ameliorate disease.
    • Given to individuals within a week of exposure to prevent disease.
  • Chronic HBV infection:
    • Can be treated with HBV polymerase inhibitors, nucleoside analogs, and interferon-alpha.
  • Vaccination is recommended for infants, children, and people in high risk groups.
    • recombinant HBsAg
46
Q

What features are seen on liver biopsy in HBV?

A

Granular eosinophilic “ground glass” appearing hepatocytes

47
Q

Hepatitis D Virus (HDV) classification:

DNA/RNA

Nucleocapsid Shape

Envelope Yes/No

Genome

Family

A
  • RNA virus
  • Icosahedral Nucleocapsid
  • Enveloped
  • SS (-) Circular Genome (Class V)
  • Deltavirus
48
Q

How is HDV transmitted?

A
  • Parenteral → Blood
  • Sexual contact
  • Perinatal → transplacentally
49
Q

What is HDV so unique?

A
  • The HDV genome is a ribozyme
    • an RNA molecule able to cleave and ligate itself
    • only known human virus to have a genome that behaves this way
50
Q

What is the route of infection in HDV?

A
  • Travels through the blood and infects hepatocytes
    • completely dependent on the presence of HBV to complete its lifecycle
    • will only replicate and release new infectious virus particles from cells that are also infected with HBV
51
Q

Why is HDV completely dependent on the presence of HBV to complete its lifecycle?

A

Requires HBsAg for packaging

52
Q

What causes the damage seen in HDV infection?

A
  • Viral antigens on the surface of HDV infected hepatocytes are recognized by the host immune system
    • leads to the activation of cytotoxic T-cells
    • Cytotoxic T-cells cause inflammation and hepatocyte necrosis
  • Tissue destruction of HBV + HDV coinfected individuals is more severe than individuals infected with HBV alone
53
Q

What is the incubation period for HDV?

A
  • Superinfection = short
    • HDV infection after HBV
  • Coinfection = long
    • HDV with HBV
54
Q

What is the clinical presentation of HDV?

A
  • Acute hepatitis
    • dependent on HBV
      • same or more severe symptoms as those associated with HBV
  • Fulminant hepatitis
    • superinfection → worse prognosis
    • 40% of all fulminant hepatitis infections
55
Q

What laboratory tests are used to diagnose HDV infection?

A

Presence of HDV can be noted by detecting the RNA genome (RT-PCR), the delta antigen, or anti-HDV antibodies (ELISA).

56
Q

What is the treatment for HDV?

A
  • No specific treatment for HDV.
  • Treating and preventing HBV infections also works to clear and prevent HDV infections.
    • Alpha-interferon → controls HBV infections which limits HDV infection
    • Vaccine → recombinant HBsAg vaccine to prevent HBV infection also blocks the establishment of HDV infections
57
Q

Hepatitis C Virus (HCV) classification:

DNA/RNA

Nucleocapsid Shape

Envelope Yes/No

Genome

Family

A
  • RNA virus
  • Icosahedral Nucleocapsid
  • Enveloped
  • SS (+) Nonsegmented Genome (Class IV)
  • Flaviviridae
58
Q

How is HCV transmitted?

A
  • Primarily blood → blood-borne pathogen
    • ​IV drug use (needle sharing)
    • Post-transfusion
      • blood transfusions prior to 1992
59
Q

What is the clinical presentation/course of HCV?

A
  • Acute hepatitis → jaundice fever
  • 70-80% of all infections become chronic infections
  • Chronic hepatitis → carrier state/asymptomatic/slowly progressing disease
    • lead to degenerative liver disease
      • cirrhosis or hepatocellular carcinoma, liver failure
  • HCV infection progresses very slowly
    • 10 to 20 years post-infection before symptoms appear
60
Q

What laboratory tests are used to diagnose HCV infection?

A
  • ELISA recognition of the anti-HCV antibody or detection of the RNA genome.
  • Genome detection, quantitation, and genotyping by RT-PCR are the gold standard for confirming the diagnosis of HCV and for planning the correct course of treatment against the infection.
61
Q

What is the treatment for HCV infection?

A
  • Recombinant interferon-alpha or pegylated interferon-alpha
  • Ribavirin: ribonucleic analog → causes genomic mutations
  • NS5A inhibitors → inhibit transcription complex
  • NS5B inhibitors → inhibit RNA polymerase (RdRp)
  • Many treatments rapidly becoming available.
62
Q

What hepatitis serologic markers does the “Acute Hepatitis Profile” test look for when diagnosing a suspected acute hepatitis?

A
  • HBs antigen
  • Anti-HBc IgM
  • Anti-HAV IgM
  • Anti-HCV (total)
63
Q

What hepatitis serologic markers does the “Chronic Hepatitis Profile (Type B)” test for when diagnosing suspected chronic hepatitis?

A
  • Chronic Hepatitis Profile (Type B) includes:
    • HBs antigen
    • HBe antigen
    • Anti-HBe (total)
64
Q

What follow up measures should be taken when a patient tests postitive for HBsAg and Anti-HBc IgM?

A
  • Test again in 3 to 6 months.
    • Looking for HBs antigen to go away and for Anti-HBs (total) to be present.
    • Sometimes this test falls in the “window” and needs to be repeated.
65
Q

What hepatitis serologic markers are different in HBV with active viral replication and HBV with non-replicating virus?

A
  • HBV (active viral replication):
    • HBs antigen = positive
    • HBe antigen = positive
    • Anti-HBe (total) = negative
  • HBV (non-replicating virus):
    • HBs antigen = positive
    • HBe antigen = negative
    • Anti-HBe (total) = positive
66
Q

What should be done in follow-up for a patient with positive active viral replication HBV?

A
  • Order a HBV DNA detection test
  • Order a serum ALT level test
    • If the ALT levels are greater than 2-fold the normal range then consider liver biopsy and start antiviral treatment.
    • Monitor treatment by HBV DNA detection tests.
67
Q

What should be done in follow-up for a patient with positive non-replicating HBV?

A
  • Order a HBV DNA detection test
  • Order a serum ALT level test
    • If you get a normal ALT result and a low HBV DNA level, continue to monitor the patient’s ALT and HBV levels.
    • If you get an elevated ALT level with a high HB DNA level suggest liver biopsy and treat with antivirals for individuals with moderate to severe inflammation or fibrosis.
68
Q

Yellow Fever Virus classification:

DNA/RNA

Nucleocapsid Shape

Envelope Yes/No

Genome

Family

A
  • RNA virus
  • Icosahedral Nucleocapsid
  • Enveloped
  • SS (+) Nonsegmented Genome (Class IV)
  • Flaviviridae
69
Q

How is Yellow Fever Virus transmitted?

A

Spread by the Aedes mosquito.

70
Q

What is the route of infection in Yellow Fever Virus?

A
  • Misquito bite → bloodstream
    • causes transient viremia
  • Blood → hepatocytes
    • directly cytolytic → direct destruction of host cells
71
Q

What are the two forms of Yellow Fever Virus?

A
  • Jungle
    • reservoir = tropical monkeys
  • Urban
    • reservoir = humans
72
Q

What is the clinical presentation of Yellow Fever?

A
  • Severe systemic disease
    • flu-like syndrome
    • loss of liver, kidney, and heart function
      • hepatitis → jaundice
    • hemorrhagic fever
    • shock
  • Mortality rate of infection can be as high as 50%.
73
Q

How is Yellow Fever diagnosed?

A
  • Immunoflorescence
  • RT-PCR
  • ELISA
  • Other various serologies
  • Direct isolation of the virus
74
Q

What is the treatment for Yellow Fever?

A
  • Supportive care
  • Vector control measures
  • Vaccination
    • Yellow Fever Virus live-attenuated vaccine
75
Q

What information should you look for in questions about viral hepatitis?

A
  • Jaundice
  • Vomiting
  • Recent travel history to regions endemic for HAV and YFV
  • Intravenous drug user
  • Blood transfusion prior to HCV screening (before 1990)
  • Vertical transmission

GI Week 5 - WLB (16 decks)

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