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GIHEP Micro - Viral Hep (ii) Hep B (transmission (in high prevalence areas…
GIHEP Micro - Viral Hep (ii) Hep B
Intro
DNA virus
infects hepatocytes + integrates into their genome make viral copies
express viral proteins on surface - triggers cellular immune response
3 forms
Dane particle (infectious form)
spherical form (no DNA, surplus viral envelope - HbsAg)
filaments (no DNA, surplus viral envelope - HbsAg)
apron 30% of world's pop has serological evidence of current or past infection
incubation period = 1-6 months (had to established as most cases are chronic @ time of dx) - long hence go back far in hx for exposure risks
transmission
perinatal
sexual
parenteral ('blood borne virus')
sharing needles - IVDUs
haemodialysis
non-sterile glucometer
sharing personal care items (toothbrush, razor)
needle stick injuries (HCWs)
piercings, tattoos, acupuncture
in high prevalence areas
intrapartum + close household contacts
acute infection in infants + young children
in low prevalence areas
acute infection sporadic + can be in adults
sexual + spread parenterally in @ risk groups
Outcomes
resolve (no longer infectious)
progress to chronic
90% of those infected in infancy progress
<5% of those infected in adulthood progress
fulminant ALF
<1%
80% mortality without OLT
Acute infection
most asymp or mild liver inflamm that resolves spontaneously
age dependent
10% of children will have symptoms
30-50% of adults will have symptoms
Chronic infection
HBsAg detectable for > 6 months
most patients = inactive carriers
symptoms may be non-specific + patients may not present until v late stages
ongoing damage -> inflamm
leads to cirrhosis in 25% of cases
leads to HCC or extra hep manifestations in 10-20% of cases
reactivation of hep B infection can occur if immunosuppressed
Serology
parts of virus
HBsAg
indicates person is CURRENTLY infectious
1st to be +ve
if +ve > 6months - chronic
HBeAg
indicates virus is actively replicating - person is HIGHLY INFECTIOUS
suggests a high viral load
can be present in acute or chronic
DNA
viral load
indicates presence of replicating virus
used to monitor + guide tx
Abs (our body's response)
Anti HBs
Ab against surface antigen
only thing to be +ve in someone vaccinated
usually last to appear + indicates resolved infection
Anti HBe
core Abs
IgM: acute
IgG: usually +ve for life
if +ve the body has been exposed to the virus itself NOT THE VACCINE
1st detectable Ab
Tx
acute: supportive tx
chronic
antivirals
aim = prevent progression to cirrhosis / liver failure / HCC
can't eradicate virus but can reduced DNA below detectable levels + seroconvert HBeAg to to Anti-HBe
monitor for HCC (US + AFP)
transplant if fulminant liver failure or end stage chronic hep
patient education
vaccination
Prevention
strategy varies in high vs low prevalence areas
standard precautions
screen blood products
clean/disposable needles
hand hygiene
PPE - gloves, goggles, apron etc
safe disposal of sharps
avoidance of risk factors (safe sex)
pre-exposure prophylaxis
cloned surface antigen (HBsAg)
develop anti HB Abs only
no Hep B core antigen so core Ab -ve
3 doses
Ab titres checked after
over 10 - protective
over 100 - ideal
for high risk groups (HCWs) + pat of national immunisation programme
post-exposure prophylaxis
Ig ASAP
for neonates, needle stick injury if no vaccine/inadequate response, after high risk sexual exposure
give vaccine too