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GIHEP Micro - Viral Hep (i) (Hep A (post-exposure prophylaxis (passive…
GIHEP Micro - Viral Hep (i)
Causes of hep
infection
viral
hep A+E (epidemiologically related)
CMV
EBV
rubella
yellow fever (in Africa + S America)
hep B+C+D (epidemiologically related)
bacterial
TB
Q fever
leptospirosis
other
non-infectious
drugs
alcohol
vasc
AI
metabolic
Hep A
RNA virus
enterovirus (picornavirus)
virus itself not cytopathic - thought that cellular immunity (CD8 T cells) cause the liver damage
transmission
human only
virus shed in faeces
primarily person-person via faecal-oral route
also - contaminated food + water
incubation period (time from infection to symptoms) = 30 days (range = 15-50)
period of infectiousness = 2wks before - 1 wks after onset of symptoms
worldwide
highest prevalence = developing countries (almost all children have Abs indicating prior infection)
countries with now better sanitation: Abs in older pop only
in developed countries
returned travellers
household or sexual contacts of known cases
IVDUs
MSM
occasional foddborne outbreaks (e.g. frozen berries in Ire - due to infected food handlers)
acute infection
asymptomatic in children
risk of symptomatic infection increase with age + co-infection (e.g. Hep B)
prodrome; symptoms for 1-2wks, followed in a few days by dark urine, pale stools, jaundice
fulminant disease (ALF) rare (<1%) - may need transplant
no chronic liver disease or carrier state (unlike hep B + C)
serology
anti-hep A virus IgM elevated during acute infection, confirms dx
protective Abs develop after infection (anti-hep A IgG) - DOES NOT INDICATE CHRONIC INFECTION, indicates past infection
PCR expensive hence not readily done (RNA only detected in acute infection, not past or vaccine)
Tx = supportive care
prevention
hygiene
sanitation
vaccination
advice to travellers (education)
pre-exposure vaccine
inactivated
for travellers to endemic countries, those with chronic liver disease, IVDUs, MSM, workers exposed to raw untxed sewage
post-exposure prophylaxis
passive immunisation (Ig)
in addition to or instead of vaccine
needs to be even within 2 wks of exposure to be effective
esp for persons aged over 50 + @ risk of severe complications (chronic liver disease incl Hep B or C)
management of cases + contacts for outbreak control
Hep E
RNA virus
4 genotypes - different geographic distribution + epidemiology
1+2: humans, transmitted via faecally contaminated water in developing countries
3 (dominent in Europe, mostly food borne) + 4: humans, pigs + other mammals
infects both humans + animals
transmission to humans
via food: undercooked/raw pig + game meat, processed pork + shellfish
directly through handing animals, esp pigs
contaminated water (poor sanitation)
incubation period = 40 days (range = 15-60)
acute infection
90% asymp
NO AGE DIFFERENTIAL (unlike hep A)
can be a/w high mortality
fulminant hep in pregnant women (20%)
genotype 1 = life-threatening to mum + foetus
usually self-limiting - symptomatic tx
chronic infection
v rare
reported in immunosuppressed patients (solid organ transplant, HIV)
can be a/w high mortality , esp liver transplant recipient with chronic infection genotype 3
tx: reduce immunosuppressive (e.g. decrease dose of anti-rejection drug) + give ribavirin
RNA in stool + blood during prodrome + up to 3 months after onset of symptoms
Serology
acute infection: IgM +ve, RNA +ve
past infection: IgG +ve, RNA -ve
prevention
hygiene
sanitation
vaccination
advice to travellers (education)
Hep D
incomplete viral particle
defective RNA virus
uses HBsAg for propagation
only causes illness with Hep B co-infection
epidemiology: 5% of patients with chronic Hep B infection are carrier
transmission: sexual, parenteral, perinatal (only possible in combo with hep B)
can be contracted @ same time as (co) or after (super) hep B
coinfection: more severe acute hep, but 90% rate of convalescence (recovery)
superinfection of a chronic HBsAg carrier: increased cirrhosis risk
in rare cases, fulminant hep
Clinical presentation of viral hep
asymp or symp
often preceded by prodromal symptoms (fever, anorexia, nausea, fatigue, RUQ pain)
dark urine - bili
pale greasy stools - need bile to absorb fats
jaundice - bili buildup
abnormal LFTs (elevated AST, ALT + bili)