A summary on the viral hepatits A-E. diagnosis and management is included.For the use of all medical students and healthcare providers.

1. Viral hepatitis
Presented by: George Wanjau
Facilitator: Dr. B.B.O Awuonda.
Date:

2. Outline
• Introduction.
• Aetiology.
• Clinical manifestations
• Investigations
• Specific viral hepatitis

3. Introduction.
• Viral hepatitis is a common cause of jaundice
and must be considered in anyone presenting
with high transaminases (LFTs)
• All these viruses cause illnesses with similar
clinical and pathological features and which are
frequently anicteric or even asymptomatic.
• They differ in their virologic characteristics,
transmission, severity, likelihood of persistence,
and subsequent risk of hepatocellular carcinoma.

4. Aetiology.
Most common. Less common. Rare.
Hepatitis A Epstein Barr Herpes simplex
Hepatitis B CMV Yellow fever.
Hepatitis C
Hepatitis D
Hepatitis E

5. Clinical manifestations of acute
infection.
• A non-specific prodromal illness characterized by
headache, myalgia, arthralgia, nausea and
anorexia usually precedes the development of
jaundice by a few days to 2 weeks.
• Vomiting and diarrhoea may follow, and abdominal
discomfort is common.
• Dark urine and pale stools may precede jaundice.
• Few physical signs. The liver is often tender but only
minimally enlarged.
• Occasionally, mild splenomegaly and cervical
lymphadenopathy are seen.(EBV)

6. Clinical manifestations of acute
infection
• Jaundice may be mild and the diagnosis may be
suspected only after finding abnormal liver blood
tests in the setting of non-specific symptoms.
• Symptoms rarely last longer than 3–6 weeks.

7. Investigations.
• LFTs
• liver enzymes
• Bilirubin
• Coagulation profile(PT time)
• FHG(relative lymphocytosis)
• Serological tests confirm the aetiology of the
infection.

8. Management.
• Most individuals do not need hospital care.
• No specific dietary modifications are needed.
• Alcohol should be avoided during the acute illness.
• Drugs such as sedatives and narcotics, which are
metabolized in the liver, should be avoided.
• Elective surgery should be avoided in cases of acute viral
hepatitis, as there is a risk of post-operative liver failure.
• Liver transplantation is very rarely indicated for acute viral
hepatitis complicated by liver failure, but is commonly
performed for complications of cirrhosis resulting from
chronic hepatitis B and C infection.

9. Hepatitis A

10. Hepatitis A- introduction
• RNA virus of Picornavirus group of enteroviruses.
• Common route of spread- Fecal-Oral, saliva.
• Rare routes include sexual, blood.
• No vertical transmission.
• No chronic disease.
• common in areas of overcrowding and poor
sanitation.
• In outbreaks water and shellfish have been the
vehicles of transmission

11. Hepatitis A: course of infection
• Infected individuals, who may be asymptomatic,
excrete the virus in faeces for about 2-3 weeks
before the onset of symptoms and then for a
further 2 weeks.
• Infection is common in children but often
asymptomatic, therefore up to 30% of adults will
have serological evidence of past infection but
give no history of jaundice.

12. Hepatitis A: investigations
• HAV is only present in the blood during the incubation period.
Excretion in the stools occurs for only 7-14 days after the onset
of the clinical illness and the virus cannot be grown readily.
ANTI-HAV (IgM type) ANTI-HAV (IgG type)
Indicates a primary immune
response
Indicates immunity to HAV
Present during onset of clinical
illness
Used to measure prevalence
diagnostic No diagnostic value
Titers fall within 3 months of
recovery
Persists years after infection

13. Management
• Treatment involves
supportive care with
complications treated
accordingly. Eg liver
transplant in
fulminant hepatic
failure (0.1%)
Prevention
• Improve social
conditions
• Immunization with
inactivated virus
vaccine
• Immune serum
globulin.- after
exposure

14. Hepatitis B

15. Hepatitis B-Introduction.
• DNA virus of
hepadna group
• Aka dane
particle
• Humans only
source of
infection

16. Hepatitis B- introduction
• Hepatitis B infection affects 300 million people
and is one of the most common causes of chronic
liver disease and hepatocellular carcinoma
world-wide.
• Acute phase often asymptomatic esp if vertically
acquired
• Chronic hepatitis, associated with elevated
serum transaminases and can lead to cirrhosis,
usually after decades of infection

17. Hepatitis B- transmission
Horizontal transmission Vertical transmission
10% risk of chronic disease 90%risk of chronic disease
Sexual transmission HbsAg-positive mother
Injected drug use
Tattoo needles
Unscreened blood products

20. Investigations- serology
• Hepatitis B surface
antigen (HBsAg) is a
reliable marker for
HBV in acute infection
• Appears in blood late
in incubation phase
and disappears after a
few days(but can last
upto 5 months)
• Antibody to HBsAg
(anti-HBs)
• Appear after 3-6 months
and persists many years
/permanently
• Imply previous infection
(Anti HBc present) or
immunization (Anti-HBc
absent)

21. Investigations- serology
• Hepatitis B core
antigen (HBcAg) is not
found in the blood
• anti-HBc appears
early in the illness and
rapidly reaches a high
titre which then
subsides gradually but
persists
• Anti-HBc is initially of
IgM type with IgG
antibody appearing
later.
• Anti-HBc (IgM) can
sometimes reveal an
acute HBV infection
when the HBsAg has
disappeared and
before anti-HBs has
developed

22. Investigations- serology
• The hepatitis B e
antigen (HBeAg)
appears only
transiently at the
outset of the illness
and is followed by the
production of
antibody (anti-HBe).
• The HBeAg reflects
active replication of
the virus in the liver

23. Chronic HBV infection- Serology
• persistence of HBsAg for longer than 6 months
• presence of HBsAg and anti-HBc (IgG) in the
blood.
• HBeAg or anti-HBe is also present
• HBeAg indicates continued relication
• anti-HBe implies that replication is occurring at a
much lower level or that HBV-DNA has become
integrated into host hepatocyte DNA.

24. Investigations- viral load
• HBV-DNA can be measured by polymerase chain
reaction (PCR)
• Viral load>105 + evidence of active replication
(HBeAG)
• Important in monitoring antiviral therapy

25. Management.
Acute infection
• supportive with
monitoring for acute
liver failure, which
occurs in less than 1%
of cases.
Chronic infection
• Indication treatment is a high
viral load in the presence of
active hepatitis
• Alfa-interferon
• Lamivudine
• Adefovir
• Tenofovit
• (MOA???)

26. prevention
• Recombinant hepatitis B vaccine containing
HBsAg- pruduces active immunity in 95%
• Ineffective in those already infected
• Administed to high risk groups E.G.????
• Intramuscular injection of hyperimmune serum
globulin prepared from blood containing anti-
HBs- post exposure (24hrs-1 week) + infants born
to positive mothers at birth

27. Hepatitis D (delta virus)
• RNA defective virus
• Depends on HBV
• Same mode of spread
• Has a world wide distribution
• Can be a simultaneous infection or a
superinfection in chronic HBV

28. Hepatitis D
• Simultaneous infection leads to a severe acute
hepatitis limited by recovery from HBV
• Superinfection in chronic HBV leads to acute
hepatitis with spontaneous recovery or even
cessation of chronic HBV
• Chronic infection with HBV+HDV can occur
leading to a rapidly progressive chronic disease

29. Investigations and managment
• Delta antigen appears
in the blood only
transiently, and in
practice diagnosis
depends on detecting
anti-HDV
• Simultaneous
infection=low
titers(IgM)
• Superinfection=high
titers(IgM->IgG)
Prevention
• Control HBV=Control
HDV

30. Hepatitis C

31. Introduction
• This is caused by an RNA
flavivirus
• Symptomatic Acute
infection is rare
• 8% individuals exposed
to the virus will become
chronically infected
• late spontaneous viral
clearance is rare.
Transmission
• Intravenous drug misuse
• Unscreened blood
products
• Vertical transmission
• Needlestick injury
• Iatrogenic parenteral
transmissionSharing
toothbrushes/razors

32. Investigations.
• Active infection is
confirmed by the
presence of serum
hepatitis C RNA in
anyone who is
antibody-positive
• Liver histology-degree
of inflammation and
fibrosis
• 6 genotypes Genotype
has no effect on
progression of liver
disease but does
affect response to
treatment

33. Management.
• The treatment of
choice is pegylated α-
interferon given
weekly
subcutaneously,
together with oral
ribavirin
• MOA???
• Liver transplantation
should be considered
when complications of
cirrhosis occur

34. Prevention and prognosis
• no active or passive protection against HCV
• Progression from chronic hepatitis to cirrhosis
occurs over 20-40 years
• Risk factors-- male gender, immunosuppression
and heavy alcohol misuse

35. Hepatitis E

36. Hepatitis E: introduction
• Rna virus
• Common in travelers
• Presentation and
transmission similar
with HAV
• Infection in pregnancy
causes acute liver
failure.
Investigations
• In acute infection IgM
antibodies to HEV are
positive
Prevention
• no active or passive
immunity to hepatitis
E

37. Questions?

38. The END.