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Viral Hepatitis Flashcards

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1
Q

Hepatitis A

A
  • Cause of:
    • Infectious hepatitis
    • Epidemic hepatitis
    • Epidemic jaundice
    • Type A hepatitis
  • Transmission is faeco-oral
    • Close personal contact
      • Household, child day care, sexual
    • Contaminated food and water
      • Food handlers, raw shellfish
    • Blood exposure - rare, IVDU or transfusion (now screened for)
  • Virus present in stool for up to 3 weeks prior to onset of jaundice
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2
Q

Hepatitis A - Virology

A
  • Key virological features:
    • First identified by electron microscopy 1973
    • RNA Picornavirus; hepatovirus
    • No envelope
    • Resistant to degradation
      • ‘Survives’ 70C for 10 mins and pH 1 room temp for 2 hrs
    • Single serotype worldwide
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3
Q

Hepatitis A - Clinical Features

A
  • Spectrum of disease from aymptomatic infection to acute liver failure
    • Many asymptomatic infections - age related (children more likely to be aymptomatic)
  • Does not cause chronic infection
  • Total anitbody to HAV develops in response to infection and confers lifelong immunity
  • Four clinical phases:
    • Incubation/ pre-clinical, 10-50 days (well, but infectious)
    • Prodromal/ pre-icteric, few days to 10 days, flu like illness, loss appetite
    • Icteric phase, fever, jaundice (pale stool & dark urine), liver enlargement and tenderness, anorexia, vomiting, fatigue, lasting 1-3 weeks
    • Convalescence
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4
Q

Hepatitis A - Rare Complications

A
  • Fulminant hepatitis
  • Cholestatis
  • Relapsing hepatitis (3-20% cases, but not after 12 months)
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5
Q

Hepatitis A - Pathogenesis

A
  • Jaundice probably due to immune mediated T lymphocyte destruction of hepatocytes
    • Not clear how this is linked to age specific rates jaundice (increases with age)
  • Fulminant hepatitis is fatal in up to 60% cases
    • Death inevitable when >80% hepatocytes killed
  • Worse prognosis if underlying liver disease
    • Chronic HBV, HCV
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6
Q

Hepatitis A - Diagnosis

A
  • Clinical
    • Biochemical features
    • Epidemiological clues (age, risk groups, travel, vaccine)
    • Difficult
  • Laboratory
    • Serology
    • Detection of IgM
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7
Q

Acute Hepatitis A - Managment

A
  • Supportive, self-limited infection
  • No antivirals
  • Check liver function, clotting, U&Es
  • Vomiting, dehydration, altered consciousness bad signs-admit
  • Transplant for acute liver failure
  • Notifiable disease
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8
Q

Hepatitis A - Prevention

A
  • Avoid risk
    • Hygiene (hand washing)
    • Clean water sources
    • Travel
  • Immunisation
    • Active: Hepatitis A vaccine (pre and post exposure)
      • Cell culture adapted virus, formalin inactivated
      • Safe, highly immunogenic, highly effective
    • Passive: Human normal immunoglobulin (HNIG) - post exposure within 14 days
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9
Q

Hepatitis A - Groups Recommended for Hepatitis A Vaccine

A
  • Injecting drug users
  • International travelers to endemic areas
  • Persons who have clotting factor disorders
  • Persons with chronic liver disease
  • Consider in men who have sex with men
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10
Q

Hepatitis B

A
  • Previously known as serum hepatitis
  • Causes acute, resolved infection
  • Can lead to chronic infection
  • Huge global burden of infection and disease
  • Transmission = typical blood borne virus
    • Sexual
    • Mother to child - signigicant in endemic regions
    • Needle sharing
    • Blood products
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11
Q

Hepatitis B - Virology

A
  • Hepadnavirus
  • ds DNA, enveloped
  • Relatively easily degraded
  • Several genotypes
    • Geographically restricted and can influence treatment outcome
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12
Q

Hepatitis B - Clinical Features

A
  • Acute and chronic infection
  • Acute resolved:
    • Asymptomatic
    • Non-specific illness
    • Hepatitis/ jaundice
      • Due to immune response
  • Chronic:
    • Evidence of chronic liver disease
      • ==> to cirrhosis and hepatocellular carcinoma (HCC)
  • Incubation period average 60-90 days (45-180)
  • Outcome of infection linked to age at infection/immune response
    • Virtually all infants and children asymptomatic
      • But much more likely to become chronic carriers
    • Up to 50% adults asymptomatic, especially likely if HIV infected
    • Acute case-fatality rate (overall) 0.5%-1%
  • If symptomatic, prodrome, icteric phase like HAV
  • May see signs of chronic liver disease
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13
Q

Hepatitis B - Complications

A
  • Premature mortality fro Cirrhosis and HCC 15-25%
  • Worldwide HBV infection accounts for:
    • 30% of all cases of cirrhosis
    • 53% of al hepatocellular carcinoma cases
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14
Q

Hepatitis B - Pathogenesis

A
  • Chronic vs. acute resolved
    • Feature of the immune response
    • Affected by:
      • Maturity
      • Immunosuppression
      • HLA type
  • HBV DNA persists in the host cell nucleus as cccDNA
    • Can also integrate into host chromosome
  • Mechanism of hepatocellular carcinoma unclear
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15
Q

Hepatitis B - Diagnosis

A
  • Clinical and epidemiological clues
  • Serology:
    • Hepatitis B surface antigen (HBsAg) ==> Infected, acute or chronic
    • Hepatitis B core IgM antibody (Anti-HBc IgM) ==> Recent infection (usually)
    • Hepatitis B core total antibody (Anti-HBc) ==> Infected at some time, may have resolved or be chronic
    • Hepatitis B e antigen (HBeAg) ==> Infected, acute or chronic with high levels of virus
    • Hepatitis B e antibody (Anti-HBe) ==> Infected at some time. If chronic, usually low levels of virus
    • Hepatitis B surface antibody (Anti-HBs) ==> Recovery from natural infection or vaccine response
    • Hepatitis B DNA (HBV DNA) ==> Partly defines need for therapy and infectivity
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16
Q

Acute Hepatitis B - Management

A
  • Supportive, antivirals not usually given
  • Check clotting, electrolytes
  • Transplant for acute liver failure
  • Counsel regarding transmission
  • Screen for other bloodborne viruses, STDs
  • Notifiable disease
    • Trace, test, and immunise relevant contacts
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17
Q

Chronic Hepatitis B

A
  • Defined as on-going infection for >6 months
  • Who to treat?
    • Guidelines evolving
      • Basically patients with viral replication causing active hepatitis:
        • e antigen positive + abnormal ALT
        • e antigen negative + abnormal LFT + HBV DNA >2,000 IU/mL
        • Other factors: coinfection HCV, HIV, cirrhosis, pregnant, starting immunosuppressive drugs
18
Q

Chronic Hepatitis B - Therapy Goals

A
  • HBV infection cannot currently be completely eliminated or “cured”
  • The clinical goal of HBV treatment:
    • Prevention or reversal of complications and death resulting from advancing severity of liver disease
      • Achieved by reducing HBV DNA levels
  • Therapies designed to suppress HBV replication are associated with biochemical remission and prevention further liver injury
  • Ideally clear HBsAg, or at least seroconvert from e Ag to e Ab
19
Q

Hepatitis B Antiviral Therapy

A
  • Immunomodulators:
    • Interferon alpha (alpha 2b, pegylated 2a)
    • Response rate 60% at best
    • Side effects
  • Nucleoside analogues
    • Lamivudine, adefovir, entecavir, tenofovir
    • Effective rapid reduction in HBV DNA
    • Antiviral resistance may develop
      • Especially to lamivudine
      • 20% at one yr, 60% at 5 yrs
      • Consider combination therapy/sequential therapy
    • Prolonged or life long therapy
  • Current first line treatments = entecavir, tenofovir, or pegylated IFN - based on disease features and patient choice
20
Q

Hepatitis B - Prevention

A
  • Avoid/ reduce risk
    • Safe sex, needle exchange, infection control
  • Screening:
    • Blood products, high risk groups, pregnancy
  • Vaccine
    • Primary prevention, post exposure
    • Universal or targeted
    • Active
      • Currently recombinant HBsAg made in yeast/bacteria
      • Not live and very safe
      • Highly immunogenic and protective
        • Protection continues even after antibody levels decline
    • Passive (HBIG)
  • Treatment of infected
21
Q

Hepatitis C - Epidemiology

A
  • Major public health problem
  • Estimates of around 200,000 people aged 15-59 years with chronic infection in England (0.3% or population)
    • Majority undiagnosed
  • Injecting drug users are the key risk group - 90% of newly acquired infections
  • Worldwide accounts for:
    • 27% of cases of liver cirrhosis
    • 25% of hepatocellular carcinoma
  • Rarely ==> death from acute liver failure
  • Major indication for liver transplant
22
Q

Hepatitis C - Transmission

A
  • Blood-borne virus
  • Percutaneous:
    • Injecting drug use
    • Clotting factors before viral inactivation/recombinant products
    • Transfusion/transplantation
    • Contaminated hospital equipment
    • Occupational needlestick (risk 1.8% from positive source)
  • Permucosal
    • Perinatal (up to 5%, no association with breastfeeding)
    • Sexual (<1% risk discordant long term couples, higher MSM)
  • 10% have no clear risk factor, temporal link lost as often present late in illness
23
Q

Hepatitis C - Virology

A
  • Flavivirus, Hepacivirus
  • Positive single stranded RNA
  • Enveloped
  • Many different genotypes
    • Distributed geographically
    • Influence treatment response
24
Q

Hepatitis C - Clinical Features

A
  • Acute resolved infection occurs, but uncommon
    • If acute icteric hepatitis occurs it is similar to that seen in HAV
  • Majority (>80%) have asymptomatic acute infection
  • Chronic infection common
  • Natural history:
    • Incubation 6-7 weeks ==>
      • Acute HCV (jaundice rare) ==>
        • Resolve 15%
        • Chronic HCV 85% ==>
          • Stable 80%
          • Cirrhosis 20% ==>
            • Slowly progressive 75%
            • HCC/liver failure 25%:
              • Ascites
              • Variceal haemmorhage
              • Jaundice
              • Encephalopathy
25
Q

Hepatitis C - Pathogenesis

A
  • Chronic or acute resolved
    • Poorly understood
    • Affected by:
      • Immunosuppression
      • HLA type
      • Viral genotype
  • Mechanism of cirrhosis and HCC:
    • Chronic inflammation
    • Immune mediated cytotoxicity
    • High cell replacement rate
  • Higher risk of severe fibrosis:
    • Increased alcohol intake
    • Age > 40 years at time of infection
    • HIV co-infection
    • Male gender
    • Chronic HBV co-infection
26
Q

Hepatitis C - Diagnosis

A
  • Usually picked up by screening risk groups or contacts or as part of liver disease work up
  • Serology - antibody or nucleic acid (RNA)
    • Seroconversion window period up to 3 months
    • Some patients never make detectable antibody - especially if immunosuppressed
27
Q

Management of Hepatitis C - General

A
  • Counsel on routes of transmission
  • Explain long-term prognosis
  • Avoid alcohol
28
Q

Management of Hepatitis C - Acute

A
  • Difficult to spot - usually asymptomatic
  • High dose IFN-alpha may reduce rate of chronicity
  • Otherwise supportive - as for HAV
  • Notifiable
29
Q

Management of Hepatitis C - Chronic

A
  • Assessment to include LFT, symptoms, liver biopsy, counsel about alcohol
  • Treat all those with moderate or worse disease - assessed by:
    • Biopsy
    • Non-invasive tests (fibroscan, biochemical marker patterns)
  • Immunise against HAV, HBV
  • Antiviral therapy
    • Goal is to clear HCV RNA
    • A sustained virological response (SVR) is associated with greatly reduced progression to cirrhosis
      • SVR is HCV RNA negative 6 months after stopping antivirals
      • 5 yr rate cirrhosis with SVR 0% vs 13% without
    • Combination antiviral therapy
      • Interferon alpha and ribavirin achieve greater response than single agents
      • Pegylated interferon and ribavirin can clear virus in up to 80% non-genotype 1 and 50% genotype 1
        • Less effective in IL28 polymorphism
      • Side effects and adherence issues - reduce efficacy
    • New Drugs:
      • Protease inhibitors - *Telaprevir, Boceprevir - *effective against genotype 1
      • Polymerase inhibitors - not genotype specific
30
Q

Hepatitis C - Virology Response

A
  • Important to monitor response to therapy and adjust treatment course accordingly
  • Various types of supoptimal response:
    • Null response = minimal changes in HCV RNA compared with baseline during the first few months of treatment
    • Partial response = HCV RNA decreases by ≥ 2 log10 copies/mL from baseline but never declines below the limit of detection
    • Breakthrough = patients initially achieve HCV RNA levels below the limit of detection but eventually experience an increase in HCV RNA on treatment to levels comparable to those observed at baseline
    • Relapse = undetectable HCV RNA for many months, including through the end of treatment, but detectable HCV RNA in the blood soon after treatment is discontinued
31
Q

Hepatitis C - Prevention

A
  • Risk reduction and counselling
    • e.g. Needle exchanges
  • Screen and test donors
  • Virus inactivation of plasma-derived products
  • Safe injection and infection control practices
  • No vaccine
32
Q

Hepatitis D - Transmission/Clinical Features

A
  • Blood borne virus:
    • Percutaneous exposure
      • IVDU
    • Permucosal exposure
      • Sexual contact
  • Satellite virus as can only propagate in the presecence of Hepatitis B virus
    • Distinguished by production of delta antigen
    • Coinfection = simultaneous transmission with HBB ==>
      • Severe acute disease
      • Lower risk of chronic infection
    • Superinfection = infection on top of chronic HBV infection or HBV carrier state ==>
      • Usually develop chronic HDV infection
      • High risk of severe chronic liver disease
33
Q

Hepatitis D - Prevention

A
  • HBV-HDV Coinfection:
    • Pre or postexposure prophylaxis to prevent HBV infection
  • HBV-HDV Superinfection:
    • Education to reduce risk behaviour among persons with chronic HBV infection
34
Q

Hepatis E - Transmission

A
  • Outbreaks typically associated with contaminated water supply/rainy season
    • Refugee camps
  • Virus in stool during incubation period and acute phase illness
  • Association with eating undercooked pork products, shellfish
  • Person to person rates low
  • Viraemic phase indicates potential for blood-borne route (rare)
  • Transplacental (in-utero) described
35
Q

Hepatitis E - Epidemiology

A
  • HEV causes large outbreaks of hepatitis in many parts of the world and sporadic cases probably worldwide
    • >50% acute viral hepatitis in epidemic regions
  • Clinico-epidemiological features:
    • UK cases imported and endemic
    • UK typical patient profile is male, over age 50yrs
    • UK indigenous HEV probably more common than HAV
    • Zoonosis? - endemic in pigs
    • High mortality in late pregnancy (up to 20%)
36
Q

Hepatitis E - Clinical Features

A
  • No chronic infection in immunocompetent (rare even in immunocompromised)
  • Incubation:
    • Mean 40 days (15-60)
  • Spectrum:
    • Asymptomatic ==> acute liver failure
  • In epidemic regions:
    • Symptomatic cases typically occur in 15-40 year age group
    • Infection of children occurs but more often asymptomatic
  • Typical natural history similar to hepatitis A, but HEV more severe:
    • Prodrome 1-7 days ==>
    • Icteric phase
    • Resolution 2-6 weeks
  • Mortality 0.5-4% (15-25% late pregnancy)
37
Q

Hepatitis E - Virology

A
  • Genome first characterised in 1990
  • Family Hepeviridae, genus Hepevirus, single serotype
  • Single stranded positive sense RNA, no envelope
  • Moderately stable
  • Four major genetic groups (genotypes) - geographically restricted:
    • 1- India, Pakistan, China, N Africa
    • 2- Mexico
    • 3- US, Europe, pigs
    • 4- China, Taiwan
38
Q

Hepatitis E - Diagnosis

A
  • (UK) Suspect on basis of exposure and exclusion of other causes
  • Serology:
    • HEV IgG/IgM
39
Q

Hepatitis E - Management

A
  • Supportive only
  • Check LFT, clotting, UE
  • Assess for signs of encephalopathy, dehydration
  • No antivirals available
  • Liver transplant for fulminant hepatitis
  • Notifiable
40
Q

Hepatitis E - Prevention

A
  • Avoid:
    • Drinking water (and ice) of unknown purity
    • Uncooked shellfish/meats
    • Uncooked fruit/vegetables not peeled or prepared by traveller
  • Vaccine
    • New vaccine produced in China

Microbiology (9 decks)

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