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Microbiology > Viral Hepatitis Cards > Flashcards

Viral Hepatitis Cards Flashcards

1
Q

Which hepatitis viruses have chronic carrier states?

A

HBV, HCB, HDV

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2
Q

What is the genome of HBV?

A

+dsDNA

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3
Q

What LFT changes are associated with acute viral hepatis?

A

AST and ALT > 1000 IU/L; GGT/Alkphos and other labs may be normal until later infection where there is damage to biliary tree, decreased synthetic function, obstruction, etc.

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4
Q

What populations/communities are associated with Hepatitis A?

A

Daycare/long-term care populations, travelers, IVDU, MSM; especially South America, Africa and Asia

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5
Q

What is the leading cause of viral hepatitis in the developing world?

A

HEV

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6
Q

What are the outcomes of HAV?

A

85% are self-limited with IgG protection; 10-15% relapse; 0.3-2% progress to fulminant hepatitis (particularly in pts with underlying liver disease)

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7
Q

What is the genetic makeup of HAV?

A

+ssRNA, non-enveloped

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8
Q

What is the genetic makeup of HEV?

A

+ssRNA, non-enveloped

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9
Q

What are the outcomes of HEV?

A

Most are self-limiting; severe in pregnancy, underlying liver disease, immunosuppressed

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10
Q

How are HAV and HEV prevented?

A

Sanitation; vaccination (e.g. HEV vaccination in China)

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11
Q

How is HBV transmitted, and who is at risk?

A

Blood/parenteral transmission; at-risk includes IVDU, healthcare workers, risky sex behavior, infants of infected mothers (perinatal) especially in endemic areas

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12
Q

Why is HBV called a pararetrovirus?

A

HBV has an incomplete dsDNA genome; it forms a complete cccDNA, is reverse transcribed to mRNA, then transcribed back into DNA.

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13
Q

How does HBV cause cell damage?

A

Adaptive immune response (cytocoxic T lymphocytes) cause hepatocyte damage/death; HBV itself is non-cytolytic

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14
Q

Describe the two types of HDV infection

A

HDV may be co-infected with HBV or may be a superinfection after HBV; superinfection causes severe hepatitis with 5-15% mortality

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15
Q

Why does HDV require HBV?

A

HDV requires HBsAg as an envelope for replication

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16
Q

How does age of transmission influence pgoression to chronic HBV?

A

Earlier age of transmission = more likely to develop chronic disease. 90% of perinatal exposures develop chronic disease; 2-10% of older children develop chronic disease.

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17
Q

What antigens/antibodies suggest acute HBV?

A

HBsAg +, HBcAb IgM+, HBeAg +, HBV DNA+, possibly HBeAb +

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18
Q

What antigens/antibodies suggest resolved HBV?

A

HBsAg+, HBcAb IgG+, HBeAb+

19
Q

What antigens/antibodies suggest immunization to HBV?

20
Q

What antigens/antibodies suggest chronic HBV infection > 6mo with HBV?

A

HBsAg+, HBcAb IgG+, HBV DNA+, possibly HBeAb or HBeAb +

21
Q

What antibodies/antigens suggest a HBV ‘window period’?

A

All negative except HBcAb IgM/G

22
Q

How is HBV prevented?

A

3-dose recombinant vaccine, 95% effective, given to newborns, children

23
Q

What are the outcomes of HBV?

A

Most are self-limited; chronic HBV increases risk for HCC and cirrhosis; fulminant hepatitis and cirrhosis require transplant

24
Q

What is the leading cause of liver transplant in the US?

A

Hepatitis C

25
What is the most common blood-borne infection in the US?
Hepatitis C
26
How is HCV transmitted, and who is at risk?
Blood/parental and body fluids; at-risk is mainly IVDU but also unsafe sex practicers
27
How does HCV cause cell damage?
Necrosis caused by cytotoxic T cells; HCV is non-cytolytic. Chronic infection may progress to cirrhosis, HCC
28
Describe the HCV genome and protein structure
ssRNA, non-enveloped; 10 viral proteins are encoded (3 structural, 7 nonstructural)
29
What are three complications of HCV?
Immune complex disease, cryoblobulinemia, vasculitis
30
What are the outcomes of acute and chronic HCV infection?
75-85% progress to chronic infection; of chronic, 20-30% progress to cirrhosis; of cirrhosis, 2-7% progress to ESLD or HCC. Only 9% achieve a sustained cure.
31
How is HCV diagnosed?
Serology detects anti-HCV Ab between 4 and 12 weeks after infection; detects 97% of cases by 6 months post-exposure. RNA PCR detects 2 weeks after exposure.
32
What is the LFT pattern in HCV?
Elevated in acute HCV; may be normal in chronic HCV.
33
Why is there no HCV vaccine?
Genetic diversity of HCV (4+ genotypes, poor proofreading and rapid replication), and neutralizing antibodies are not protective.
34
What group in the US is most likely to have undiagnosed HCV?
Adults born between 1946 and 1965
35
What is the second generation HCV treatment?
NS5A inhibitor and HS5B inhibitor; 100% cure rate of HCV genotype 1 in 8 weeks
36
What is the first generation treatment for HCV?
Protease inhibitors + interferon and ribavirin; 80% cure rate
37
Describe the effectiveness of interferon+ribavirin
Used in the 1990s to treat HCV due to broad antibiral properties. Genotype 2 and 3 responded well, while GT1 responded only 50% of the time.
38
Describe the genotype frequencies in HCV
70% of strains are GT1 (1a>1b), 30% have GT 2 or 3, and 1% have GT4. Treatment will vary depending on genotype.
39
What antibody titer suggests an acute Hepatitis A infection?
Hepatitis A IgM antibody
40
Who is at highest risk of becoming a chronic Hepatitis B carrier?
Infants or young children
41
What antibody titer suggests a past Hepatitis A infection?
Hepatitis A IgG antibody
42
What is the most common mode of Hepatitis A transmission?
Fecal-oral (contamination of food or water)
43
When does shedding of infectious Hepatitis A particles begin?
2 weeks before symptom onset, and extends 1 week after sympoms abate
44
What is the best way to detect an early Hepatitis C infection (
HCV RNA in serum via PCR

Microbiology (9 decks)

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