1
Acute hepatitis
Dr.TARIKU D 12/13/2024
2 Out line
Epidemiology and virology of different hepatotrophic virus
Transmission of different hepatotrophic virus
General clinical presentation of acute hepatitis
Complication of acute hepatitis
Treatment of acute hepatitis
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How to prevent hepatitis
3 Acute hepatitis
commonly cause is viral hepatitis
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Hepatitis A Virus: Morphology and Characteristics
4 Hepatitis A Virus
· Nucleic Acid: ssRNA
27 nm · Classification: genus Picornaviridae,
family Hepatovirus
· One serotype and multiple
genotypes
· Nonenveloped, acid and heat stable
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Global Prevalence of Hepatitis A
HAV - Epidemiology
5
Global Prevalence of Hepatitis A
Infection
HAV
HAV Prevalence
Prevalence
High
High
Intermediate
Intermediate
Low
Low
Very
Very Low
Low
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Routes of Hepatitis A Transmission
6
Hepatitis A Transmission
· Close personal contact
0 Household or sexual contact
0 Daycare centers
· Fecal-oral contamination of food or water
0 Food handlers
0 Raw shellfish
0 Travel to endemic areas
· Blood-borne (rare)
0 Injecting drug users
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HAV
7
Typical Serologic Course of Acute
Hepatitis A Virus Infection
Sympto
ms
ALT anti-HAV
Fecal
Fecal
HAV
HAV IgM anti-HAV
0
0 1
1 2
2 3
3 4
4 5
5 6
6 12
12 24
24
Dr.TARIKU D Months after exposure 12/13/2024
HAV
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Clinical Variants of Hepatitis
A Infection
· Asymptomatic (anicteric) disease
0 Children under 6 years of age, > 90%
0 Children from 6-14 years old, 40-50%
· Symptomatic (icteric) disease
0 Adults and children over 14, 70-80%
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HAV
9
Clinical Variants of HAV
Infection
· Cholestatic hepatitis
· Relapsing hepatitis
· Fulminant hepatic failure
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10 Hepatitis B
HBV is a DNA virus with a remarkably compact genomic
structure; despite its small size and circular shape
HBV DNA codes for four sets of viral products with a
complex, multi-particle structure.
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Virology
The S gene encodes the viral surface
11
envelope protein (hepatitis B surface
antigen, HBsAg) and is composed of the
pre-S1, pre-S2, and S regions.
• The core gene (C) consists of the
precore (Pre-C) and core regions, which
give rise to the hepatitis B e antigen
(HBeAg) and core protein,
respectively.
• The polymerase (P) gene overlaps the
entire S gene
• The fourth gene (X) codes for an
incompletely understood protein,HBX.
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12 Genotypes
A genetic classification based on comparisons of complete
genomes has demonstrated 10 genotypes (designated A through J)
and numerous subtypes of HBV
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13 Epidemiology
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14ROUTE OF TRANSMISSION
Needle stick: occupational, non occupational
IV drug injection
Organ transplantation
Blood products transfusion
Sexual transmission
Vertical transmission
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15 Serology
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16
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17
Dr.TARIKU D 12/13/2024
Risk of chronic infection
Risk of Chronic Infection
100
80
60
%
%
Risk
40
20
0
Neonates Infants Children Adults
Age at Infection
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18
Clinical Features
19
Incubation 60-90 days (range 45-180)
Jaundice relatively uncommon in children
Acute mortality 0.5-1%
Chronic infection common, age-related
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Hepatitis D Virus: Morphology and Characteristics
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· Nucleic Acid: ssRNA
· Classification: unclassified,
related to viroids; deltavirus
· Is called defective virus
· HBV envelope
35-37nm · One serotype, three genotypes
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HDV
Modes of HDV infection
21 Coinfection
B
B
D
D
Superinfection
B
B
D
D
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HDV
22
HDV - Coinfection
ALT
HDV RNA
IgM anti-HDV IgG anti-HDV
HDAg
IgM anti-HBc IgG anti-HBc
HBsAg anti-HBs
Months
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Hepatitis C virus (HCV)
23
RNA virus of the Flaviridae family.
transmitted parenteraly (most commonly), multiple sexual partner,
sharing of sharp materials and perinatal transmission is (4%)
Before universal screening of the blood supply in the United
States, which began in 1990, HCV was the most common cause of
post transfusion.
Has 6 genotype
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24
acute HCV infection is more likely to be asymptomatic than is acute HAV
or HBV infection.
Incubation period 15-160 days (7 week)
Only 10% to 20% of patients with acute HCV infection develop jaundice
only 20% to 30% have nonspecific symptoms of fatigue, nausea, or
vomiting.
in jaundiced patient , the bilirubin level usually peaks at less than 10 to 15
mg/dl, and peak serum aminotransferase levels are usually under 1,000
units/L.
ProgressionDr.TARIKU
to fulminant
D
liver failure is exceedingly rare 12/13/2024
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Most untreated cases of acute hepatitis C (50% to 84%) will
evolve into chronic HCV infection.
Spontaneous recovery is more likely to occur in patients who
have
an icteric illness,
those infected with HCV genotype 2 or 3
those who experience rapid decline in HCV RNA levels during the
first 4 weeks.
When spontaneous recovery occurs, it usually does so within
the first 3 to 4 months of infection.
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26 Serology
HCV PCR detectable after 2 wk infection
Anti HCV ab detectable between 7 to 8 wk may take up to 12 wk
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27 Screening
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28 Hepatitis E virus (HEV)
is an RNA virus that is transmitted through the fecal-oral
route.
Contaminated water sources are responsible for most large
outbreaks.
Thus, hepatitis E is endemic in developing areas with warm
climates, such as India, Asia, Central America, Africa, and the
Middle East..
No vaccine for HEV is available as of yet, but good sanitation
and personal hygiene may help curtail outbreaks.
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The incubation period of HEV infection is 28 to 40 days
Serum aminotransferase levels peak 42 to 46 days after exposure
Hepato-splenomegaly and pruritus are not uncommon
Acute hepatitis E may progress to fulminant liver failure.
The overall mortality is less than 1%.
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the mortality from hepatitis E is much higher in pregnant women, and it
increases with the duration of pregnancy
Maternal mortality is about 1% to 2% in the first trimester, 8% to 10% in the
second trimester, and 20% in the third trimester
Patients with underlying chronic liver disease also have very high
mortality (up to 67%)
Survivors of hepatitis E do not develop chronic infection
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31 Serology
IgM HEV
Earlier can be negative till ALT rise so repeat in high suspicion
Stay for 6 mn
RNA HEV
Detectable after 2 wk of infection
IgG HEV
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32 General clinical picture
The prodromal symptoms of acute viral hepatitis are systemic
and quite variable.
Constitutional symptoms
anorexia, nausea and vomiting, fatigue, malaise,
arthralgia, myalgia, headache, photophobia, pharyngitis,
cough, and coryza may precede the onset of jaundice by 1–2 weeks.
The nausea, vomiting, and anorexia are frequently associated
with alterations in olfaction and taste.
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33 Cont’d
fever between 38° and 39°C in hepatitis A and E than in
hepatitis B or C, except when hepatitis B is heralded by a
serum sickness–like syndrome
Dark urine and clay-colored stools may be noticed by the
patient from 1–5 days before the onset of clinical jaundice.
With the onset of clinical jaundice, the constitutional
prodromal symptom diminish
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34
Tender hepatomegaly with RUQ pain
cholestatic picture, suggesting extrahepatic biliary
obstruction.
Splenomegaly and cervical adenopathy are present in 10–
20% of patients with acute hepatitis.
Rarely, a few spider angiomas appear during the icteric
phase and disappear during convalescence.
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35
Recovery phase
usually some hepatomegally and abnormalities in liver test are still
evident.
Post icteric phase
Duration is variable ,ranging from 2–12 weeks, and is usually more
prolonged in acute hepatitis B and C.
Complete recovery is to be expected (clinical and biochemical)
1–2 months after all cases of hepatitis A and E and
3–4 months after the onset of jaundice in three-quarters of
uncomplicated,
hepatitis B is self-limited in 95–99%, whereas hepatitis
C is self limited in only ~15%).
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In the remainder, biochemical recovery may be prolonged
36 Investigation
CBC neutropenia transient
AST and ALT (400-4000u/l)
Bilirubin mixed increment
PT marked prolongation has poor prognosis
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37 Serology
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38 Complication
Relapsing hepatitis Hep A
Cholestatic Hepatitis Hep A
serum sickness syndrome :-
During the prodromal phase of acute hepatitis B, a serum sickness–
like syndrome characterized by arthralgia or arthritis, rash,
angioedema, and rarely, hematuria and proteinuria may develop in
5–10% of patients
Fulminant hepatitis
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Fulminant hepatitis
39
Is development of HE 8 wk after liver disease symptom or
development of HE after 2 wks jaundice inpatient with no previous n
liver disease
Seen commonly in
HBV,HDV and HEV
In HAV when there is already CLD and in elderly
rarely in HCV
HBV result > 50 % of fulminant hepatitis including with HDV co-
infection
HEV in 1-2 % and in pregnant 20 %
Mortality is 80%
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Treatment liver transplant
40
Chronic hepatitis
following features suggest progression of acute hepatitis to chronic
hepatitis:
Lack of complete resolution of clinical symptoms
the presence of bridging/interface or multilobular hepatic necrosis on liver
biopsy during protracted, severe acute viral hepatitis
failure of the serum aminotransferase, bilirubin, and globulin levels to
return to normal within 6–12 months after the acute illness; and
the persistence of HBeAg for >3 months or HBsAg for >6 months after
acute hepatitis
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41
Rare complications of viral hepatitis include
pancreatitis, myocarditis, atypical pneumonia, aplastic anemia,
transverse myelitis, and peripheral neuropathy
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42 Treatment
General measure
Avoid hepatotoxic drugs
High calorie diet
For sever hepatitis hospital admission
For hepatitis B antiviral for fulminant hepatitis given for 3mn
after HBsAg conversion and 6 month after HBeAg conversion
Acute HCV can use DAAS( Eg.safusbuvir and ledispasvir) for 8
wk
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43
Fulminant hepatitis
Supportive care
Management of hepatic encephalopathy
Mannitol
Last option liver transplant
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44
prevention
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45
Hepatitis A: Pre-exposure Vaccination
Persons at increased risk or danger of infection
· Travelers to intermediate and high
HAV prevalence areas
· Injecting drug users
· Persons with chronic liver disease
· Routine pre-school childhood vaccination
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46 Prevention
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47
Hepatitis A Prevention - Immune
Globulin
Preexposure
Preexposure
· Travelers to high HAV-prevalence
regions
Postexposure
Postexposure (within
(within 14
14 days)
days)
· Routine
· Household and other intimate contacts
· Selected situations
· Institutions (e.g. daycare centers)
· Common source exposure (e.g. food
prepared by infected food handler)
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48 Prevention for HBV
Immunoglobin
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Summary
49
There are different causes for acute hepatitis common are hepato-trophic virus
HAV and HEV result only acute hepatitis and are transmitted feco-oral
Patient mostly present with non specific symptom
IgM antibodies used to make diagnosis
Feared complication is fulminant hepatitis
Treatment is supportive care unless the patient has fulminant hepatitis
Prevention with vaccination important
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50
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51
Thank you
Dr.TARIKU D 12/13/2024
