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Hepatitis means inflammation and damage to the
liver, and has differing aetiologies including:
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Other viruses causing hepatitis include:
Cytomegalovirus
Enteroviruses
Viral hepatitis type A (VHA)
Family – Picornaviridae
Genus – Hepatovirus
Pathogenesis of VHA:
* HAV spreads from person to person by:
- close contact (poor hand hygiene)
- contamination of food or water (raw oysters)
- intimate contact (anal intercourse)
* route of infection = fecal-oral route (mainly)
* principal age distribution = children and young adult
Clinical features:
- sudden onset of fever with anorexia, nausea
vomiting and jaundice (more common in adult)
Complications:
- uncommon, complete recovery, no chronicity
no carrier state
Laboratory diagnosis:
Specimen:
Stool (2 weeks before and after jaundice)
Blood (2 weeks before and 1 week after jaundice)
Pathogenesis of VHE:
• Spreads by fecal-oral route
• Incubation period is 6 – 8 weeks
• The disease is generally mild.
• Virus is eliminated from the body on recovery
• No carrier-state
Complication:
The disease is severe in pregnant women, with a high
mortality, up to 20% during the third trimester due to
fulminant hepatitis.
Laboratory diagnosis:
- by serological tests to detect HEV specific IgM
Epidemiology:
HBV is worldwide in
distribution.
Modes of transmission
and response to infection vary, depending on the age at
time of infection.
Structure and composition:
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Pathogenesis of VHB:
Modes of transmission:
1) Parenteral transmission
- transfusion of infected/ contaminated blood
- transfusion with contaminated needle,
syringe or infusion set, (needle stick injury)
2) Sexual transmission
- heterosexual/homosexual/bisexual
3) Vertical transmission (from infected mother to
- fetus via placental transmission (prenatal)
- fetus contact with vaginal secretion (perinatal)
- infant via mother’s breast milk (postnatal)
HBs Ag can be detected in saliva, naso-pharyngeal
washings, semen, menstrual fluid.
Transmission from carriers to close contacts by the oral
route or by other intimate exposure occurs.
Incubation period = 50 – 180 days
(Avg. 60 – 90 days)
After entering the body, the virus reaches the blood,
then the liver, where the result is inflammation and
necrosis.
Much of the pathology is immune mediated, as infected
liver cells are attacked by virus specific cytotoxic T cells.
The immune response slowly becomes effective, virus
replication is reduced and eventually, although
sometimes not for many months, the blood become
non-infectious.
Clinical features:
- insidious onset
- fever (less common), jaundice
- nausea, vomiting and anorexia
- skin rash
- polyarthritis due to circulating
- glomerulonephritis immune complex
Clinical outcomes of acute HBV infection
Laboratory diagnosis of VHB:
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Serum Glutamate-Pyruvate
Transaminase (SGPT) also known as
Alanine Transaminase (ALT)
recombinant interferon-
antiviral drugs
Lamivudine single or combine therapy
Adefovir for long duration
Liver transplant for chronic hepatitis with end-stage
liver damage.
Prevention and control:
1) General measures:
- aware of modes of transmission
2) Specific measures:
* Pre-exposure prophylaxis
Active immunization by hepatitis B vaccine
- plasma derived hepatitis B vaccine
- recombinant hepatitis B vaccine
- polypeptide vaccine (22nm particles.)
- recombinant of live vaccinia virus and the
HBsAg gene
Active immunization to:
newborn babies
health care workers/ laboratory personal
Post-exposure prophylaxis
Specific hepatitis B immune globulin (HBIG)
Epidemiology:
Epidemiology:
Infections by HCV are extensive throughout the world.
The World Health Organization estimated in 1997 that
about 3% of the world population has been infected.
Serological tests
detection of HCV antibody (EIA)[can not distinguish
among acute, chronic or resolved infection]
qualitative and quantitative HCV RNA detection
Genotype analysis
Treatment:
Pegylated INF combined with ribavirin, telaprevir or
boceprevir
Liver transplant for chronic hepatitis with end-stage
liver damage.
No vaccine is available for prevention
Viral hepatitis type F:
Hepatitis F is a hypothetical virus linked to hepatitis.
That novel viral particles had been discovered in the stool
of post-transfusion patients.
Viral hepatitis type G:
It is also known as GB virus C (GBV-C)
GBV-C infection has been found worldwide and currently
infects approximately one sixth of the world's
population.
High prevalence is observed among subjects with the risk
of parenteral exposures.
Sexual contact and vertical transmission may occur.
Transfusion-transmitted virus (TTV)
Viral hepatitis non A – G
Non-A-G hepatitis consists of all of the hepatitis viruses
References:
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