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Presented By:- Himanshu Dev
DMLT VI th Sem.
VMMC & SJH
What is Viral Hepatitis?
 Viral hepatitis is a systemic disease with primary
inflammation of the liver by any one of a heterogeneous
group of hepatotropic viruses.
 The most common causes of viral hepatitis are the five
unrelated hepatotropic viruses Hepatitis A, Hepatitis
B, Hepatitis C, Hepatitis D, and Hepatitis E.
 In addition to the nominal hepatitis viruses, other viruses
that can also cause liver inflammation include Herpes
simplex, Cytomegalovirus, Epstein–Barr virus, or Yellow
fever.
 Clinical Terms
 Hepatitis: inflammation of liver;
 Acute Viral Hepatitis: symptoms last less than 6 months
 Acute Hepatic Failure:is the appearance of severe complications rapidly
after the first signs of liver disease (such as jaundice), and indicates
that the liver has sustained severe damage (loss of function of 80-90% of
liver cells).Massive hepatic necrosis with impaired consciousness within
8 weeks of onset of illness.
 Chronic Hepatitis: Inflammation of liver for at least 6 months
 Cirrhosis: Replacement of liver tissue fibrosis(scar tissue).These
changes lead to loss of liver function.
 Fulminant Hepatitis: severe impairment of hepatic functions or severe
necrosis of hepatocytes in the absence of preexisting liver disease.
Viral Hepatitis- Historical Perspective
A“Infectious”
“Serum”
Viral hepatitis
Enterically
transmitted
Parenterally
transmitted
G
E
NANB
B D C
 Types Of Viral Hepatitis
Viral Hepatitis A Viral Hepatitis B Viral Hepatitis C Viral Hepatitis D Viral Hepatitis E
Agent Hepatitis A virus
(HAV); ssRNA;
No envelope
Hepatitis B virus
(HBV); dsDNA;
envelope
Hepatitis C virus
(HCV); ssRNA;
envelope
Hepatitis D virus
(HDV); ssRNA;
envelope from
HBV
Hepatitis E virus
(HEV); ssRNA;
no envelope
Route of
Transmission
Fecal-oral Parenteral,
Vertical, Sexual.
Parenteral Parenteral Fecal-oral
Age affected Children Any age Adults Any age Young adults
Carrier state Nil Common Present Nil (only with
HBV)
Nil
Incubation period 10-50 days (avg.
25-30)
50-180 days
(avg. 60-90)
40-120 days 2-12 weeks 2-9 weeks
Chronic infection No Yes Yes Yes No
Specific
Prophylaxis
Ig and Vaccine Ig and Vaccine Nil HBV vaccine Nil
Hepatitis A
 Hepatitis A (formerly known as ―infectious‖ hepatitis
or epidemic jaundice) is an acute infectious disease
caused by Hepatitis A virus (HAV).
 The disease is heralded by non-specific symptoms
such as fever, chills, headache, fatigue, generalized
weakness and aches and pains, followed by
anorexia, nausea, vomiting, dark urine and jaundice.
 The disease is benign with complete recovery in
several weeks.
 Epidemiological determinants
Agent factors
a) AGENT: The causative agent, the
hepatitis A virus, is an enterovirus of
the Picornaviridae family. It
multiplies only in hepatocytes.
b) RESISTANCE: The virus is fairly
resistant to heat and chemicals.
-Withstands heating to 600 C for 1 hr.
and is not affected by chlorine in
doses usually employed for
chlorination.
-Formalin is stated to be an effective
disinfectant.
-The virus is inactivated by
ultraviolet rays and by boiling for 5
minutes or autoclaving.
RNA
Naked RNA virus
c) RESERVOIR OF INFECTION: The human cases are the only
reservoir of infection.
d) PERIOD OF INFECTIVITY : The risk of transmitting HAV is
greatest from 2 weeks before to 1 week after the onset
of jaundice.
e) INFECTIVE MATERIAL : Mainly man’s faeces.
f) VIRUS EXCRETION: HAV is excreted in the faeces for
about 2 weeks before onset of jaundice and for up to 2
weeks thereafter.
Host factors
a) AGE: Infection with HAV is more frequent among children than in
adults. However, people from all ages may be infected if susceptible.
b) SEX: Both sexes are equally susceptible.
c) IMMUNITY: Immunity after attack probably lasts for life.
Environmental factors
 Cases may occur throughout the year.
 In India the disease tends to be associated with periods of heavy
rainfall.
Mode of Transmission
Incubation period
10-50 days (usually 25 to 30 days).
a) FAECAL-ORAL ROUTE: Major route of transmission.
-By contaminated water, food or milk.
b) PARENTERAL ROUTE (Rarely):
-By blood and blood products or by skin penetration through
contaminated needles.
c) SEXUAL TRANSMISSION:
-May occur mainly among homosexual men because of oral-anal
contact.
Diagnosis
1. Demonstration of Virus in feces, blood, bile:
By: Immunoelectron microscopy
2. Virus Isolation:
3. Detection of Antibody :By ELISA
4. Biochemical tests:
i) Alanine aminotransferase (ALT)
ii) Bilirubin
iii) Protein
5. Molecular Diagnosis : RT PCR of feces
Prevention:-
-hygienic measures and sanitation
-passive immunization(Human Immunoglobulin
Gamma globulin given before exposure to virus
or early during the incubation period, will
prevent or attenuate a clinical illness.
-active immunization
Several inactivated or live attenuated vaccines
against hepatitis A have been developed.
Treatment:
-nospecific, dietary food and long rest
Hepatitis B
Hepatitis B (formerly known as ―serum‖ hepatitis)
is an acute systemic infection with major pathology
in the liver, caused by hepatitis B virus.
Transmitted by the Parenteral route.
The acute illness causes liver inflammation, vomiting,
jaundice, and, rarely, death. Chronic hepatitis B may
eventually cause cirrhosis and liver cancer.
Hepatitis B is endemic throughout the world,
especially in tropical & developing countries.
Epidemiology Determinants
Agent factor
a) AGENT: Hepatitis B Virus (HBV)
-It is a complex, 42 nm double-shelled DNA virus originally known
as ―Dane Particle‖.
-It replicates in liver cell.
HBV occurs in 3 morphology form in serum:
i. Small spherical particles with an average Diameter of 22nm.
ii. Filamentous or Tubules of varying length & of 22 nm diameter.
iii. Dane particle.
Out of 3 morphology forms, only the Dane particle is considered infectious, other
circulating morphology forms are not infectious.
HBV : Structure
Dane particle
b) RESERVOIR OF INFECTION:
-Men is the only reservoir of infection which can be spread either from carriers or
from cases.
c) Infective material:
-Contaminated blood is the main source,
-Virus has been found in body secretion such as saliva, vaginal secretion & Semen
in infected material.
d) Resistance:
-Readily destroyed by sodium hypochlorite, as is by heat sterilization in
an autoclave for 30-60 min.
Host factor
a) AGE:
-Acute hepatitis B
90% resolve by themselves; <1% develop
fulminant hepatic failure.
-occurs in approx.:
Perinatal -1%
Childhood -10%(1-5 yr. age)
Late infection -30%(>5 yr. age)
-Chronic hepatitis B
2-10% progress to chronic state.
-occur in approx.
Perinatal -95%
Childhood -80%
After 5 yr. of age -5-10%
b) High Risk Group:
 People from endemic regions
 Babies of mothers with chronic HBV
 Intravenous drug abusers
 People with multiple sex partners
 Hemophiliacs and other patients requiting blood and
blood product treatments
 Health care personnel who have contact with blood
 Patients who are immunocompromised.
c) Humoral and cellular response:
-HBV has 3 distinct antigen:
i. HBsAg, also known as ―Australian antigen,
ii. HBcAg antigen (core antigen)
iii. HBeAg envelope antigen
They stimulate production of corresponding antibody.
Incubation Period
45-180 days (usually 60-90 days)
Mode of Transmission
 Parenteral- IV drug abusers, health workers are at
increased risk.
 Sexual- sex workers and homosexuals are particular at
risk.
 Perinatal (Vertical) – mother (HBeAg+) →infant. Mothers
who are HBeAg positive are much more likely to transmit
to their offspring than those who are not. Perinatal
transmission is the main means of transmission in high
prevalence populations.
Diagnosis
 Serology
 Liver Chemistry tests
AST, ALT, ALP, and total Bilirubin
 Histology--Immunoperoxidase staining
 HBV Viral DNA--Most accurate marker of viral
DNA and detected by PCR
 Liver Biopsy--to determine grade(Inflammation)
and stage(Fibrosis) in chronic Hepatitis
1) HBsAg :- It is the first marker to appear in blood after infection.
2) Anti-HBs(HBsAb) :-Disappearance of HBsAg and the appearance of anti-HBs
signals recovery from HBV infection, non-infectivity.
3) Anti-HBc :- IgM anti-HBc appears shortly after HBsAg is detect (HBcAg alone
dose not appear in serum)
IgM-HBc may also or can persist for 3-6 months or longer.
IgG-HBc also appear during acute hepatitis B but persist indefinitely.
4) HBeAg :-
HBeAg appear in blood concurrently with HBsAg, or soon afterwards.
HBeAg is a soluble protein found only in HBeAg positive serum.
HBeAg indicate viral replication and infectivity.
Persistence of HBeAg in serum beyond 3 month indicate an increased like
hood of chronic hepatitis B.
Serologic Events
concentration
Weeks post infection
HBsAg
HBeAg
Anti-HBc
Anti-HBs
Anti-HBeAnti-HBc
IgM
8 12 16 20 24 28 32 36 40 44 52
ALT
Symptoms
Virus/Antibody markers
Interpretation
HBsAg HBeAg Anti-HBc Anti-HBs Anti-HBe
+ + IgM - -
Acute HBV infection; highly infectious
+ + IgG - -
Late/Chronic HBV infection or carrier
state; highly infectivity
+ - IgG - +/-
Late/Chronic HBV infection or carrier
state; low infectivity
- +/- IgM - +/-
Seen rarely in early acute HBV
infection; infectious
- - IgG +/- +/-
Remote HBV infection; infectivity nil
or very low
- - - + -
Immunity following HBV vaccine
Interpretation of common serological patterns in HBV infection
Prevention
 Vaccination
- highly effective recombinant vaccines
 Hepatitis B Immunoglobulin (HBIG)
-exposed within 48 hours of the incident/ neonates
whose mothers are HBsAg and HBeAg positive.
 Other measures
-screening of blood donors, blood and body fluid
precautions.
National Immunization Schedule
Vaccine When to Give Dose Route Site
Hepatitis B At birth or as
soon as
possible with
in 24 hours.
0.5 ml IM Antero lateral
side of mid
thigh
Hepatitis B
1,2,3
At 6, 10, 14
weeks
0.5 ml IM Antero lateral
side of mid
thigh
Treatment
 Interferon Alfa (Intron A)
Response rate is 30 to 40%.
 Lamivudine (Epivir HBV)
(relapse ,drug resistance)
 Adefovir dipivoxil (Hepsera)
Hepatitis C
 Hepatitis C is an infectious disease affecting primarily
the liver, caused by the hepatitis C virus (HCV).
 The infection is often asymptomatic, but chronic infection
can lead to scarring of the liver and ultimately to cirrhosis,
which is generally apparent after many years.
 It is estimated that 150–200 million people, or ~3% of the
world's population, are living with chronic hepatitis C.
 HCV infection is prevalent in India too, with an estimated
12.5 million cases.
 Overt jaundice is seen in about 5 % of patients only.
 The important part in type C hepatitis is the chronic illness.
 About 50 to 80 % of patients progress to chronic hepatitis.
Hepatitis C Virus
 HCV is a 50-60 nm virus with a linear,
single stranded RNA genome,
enclosed with in a core and
surrounded by an envelope, carrying
glycoprotein spikes.
 It is a member of
the Hepacivirus genus in the
family Flaviviridae.
 The half life of the virus particles in
the serum is around 3 hours and may
be as short as 45 minutes.
 In addition to replicating in the liver
the virus can multiply in lymphocytes.
Incubation Period
40-120 days
Mode of Transmission
 Intravenous Drug Use
 Healthcare Exposure: Blood Transfusion, transfusion of Blood products,
Organ Transplant without HCV screening carry significant risk of infection.
 Hemodialysis
 Accidental injuries with needles/sharps
 Sexual/household exposure to anti-HCV-positive contact
 Multiple sex partners
 Vertical Transmission: Vertical transmission of hepatitis C from an infected
mother to her child
Symptoms
anti-
HCV
ALT
Normal
0 1 2 3 4 5 6 1 2 3 4
Hepatitis C Virus Infection
Typical Serologic Course
Titre
Months Years
Time after Exposure
• HCV antibody – ELISA used to diagnose hepatitis C infection.
Not useful in the acute phase as it takes at least 4 weeks
after infection before antibody appears.
• HCV-RNA - various techniques are available e.g. PCR and
branched DNA. May be used to diagnose HCV infection in
the acute phase. However, its main use is in monitoring the
response to antiviral therapy.
• HCV-antigen - an EIA for HCV antigen is available. It is used
in the same capacity as HCV-RNA tests but is much easier to
carry out.
Diagnosis
Prevention
 Only General Prophylaxis, such as blood, tissue, organ screening, is possible.
 No specific active or passive immunizing agent is available.
Treatment
Interferon - may be considered for patients with chronic active hepatitis.
The response rate is around 50% but 50% of responders will relapse upon
withdrawal of treatment.
Ribavirin - there is less experience with ribavirin than interferon.
However, recent studies suggest that a combination of interferon and
ribavirin is more effective than interferon alone.
Hepatitis D
 Hepatitis D, also referred to as hepatitis D virus (HDV)
and classified as Hepatitis delta virus, is
a disease caused by a small circular enveloped RNA virus.
 HDV is considered to be a subviral satellite because it can
propagate only in the presence of the hepatitis B
virus (HBV).
Hepatitis D virus
VIRION: spherical, 36-38
nm particle with an outer
coat composed of the
HBsAg surrounding ssRNA
genome.
Satellite virus : replicates
only in the presence of
HBV
Incubation Period
2-12 weeks
Mode of Transmission
The primary route of Transmission are believed to be
similar to those of HBV, though HDV does not appear to
be sexually transmitted disease.
Clinical Features
 Infection is dependent on HBV replication, as HBV provides an HBsAg
envelop for HDV.
 Two types of infection are recognisesd, coinfection and superinfection.
In Coinfection, delta and HBV are transmitted together at the same time.
In Superinfection, delta infection occurs in a person already harbouring HBV.
Diagnosis
 Delta antigen is primarily expressed in liver cell nuclei, where it can
be demonstrated by immunofluorescence.
 Anti-delta antibodies appear in serum and can be identified by
ELISA.
IgM antibody appears 2-3 weeks after infection and is soon replaced
by the IgG antibody in acute delta infection.
anti-HBs
Symptoms
ALT Elevated
Total anti-HDV
IgM anti-HDV
HDV RNA
HBsAg
HBV - HDV Coinfection
Typical Serologic Course
Titre
Time after Exposure
Jaundice
Symptoms
ALT
Total anti-HDV
IgM anti-HDV
HDV RNA
HBsAg
HBV – HDV Superinfection
Typical Serologic Course
Time after Exposure
Titre
 HBV-HDV Coinfection
Pre or post exposure prophylaxis to prevent HBV
infection. Screening of blood donor for HBsAg.
 HBV-HDV Superinfection
Education to reduce risk behaviors among persons with
chronic HBV infection.
Prevention
Hepatitis E
 Hepatitis E is a viral hepatitis (liver inflammation) caused by infection with
a virus called hepatitis E virus (HEV).
 Although Hepatitis E often causes an acute and self-limiting infection (in
that it usually goes away by itself and the patient recovers) with low
mortality rates.
 It bears a high risk of developing chronic hepatitis in immunocompromised
patients with substantial mortality rates.
 Hepatitis E occasionally develops into an acute, severe liver disease, and is
fatal in about 2% of all cases.
 In pregnant women the disease is more often severe and is associated with
a clinical syndrome called fulminant hepatic failure.
Signs and Symptoms
Acute Infections:
The incubation period of hepatitis E varies from 3 to 8 weeks.
After a short prodromal phase symptoms lasting from days to
weeks follow. They may include jaundice, fatigue and nausea.
Viral RNA becomes detectable in stool and blood serum during
incubation period.
Serum IgM and IgG antibodies against HEV appear just before
onset of clinical symptoms.
Recovery leads to virus clearance from the blood, while the virus
may persist in stool for much longer.
Recovery is also marked by disappearance of IgM antibodies and
increase of levels of IgG antibodies.
Chronic Infections:
While usually an acute disease, in immunocompromised subjects—
particularly in solid organ transplanted patients—hepatitis E may
cause a chronic infection.
Occasionally this may cause liver fibrosis and cirrhosis.
Hepatitis E virus
 HEV is spherical nonenveloped virus, 29-nm to 32 nm
in diameter, with a ssRNA genome.
 The surface of the virion shows indentation and
spikes.
 The Virus is very labile.
 II has been classified in the genus Herpes virus under
the family Caliciviridae.
Incubation Period
2-9 weeks
Animal Reservoir: Pigs
Mode of Transmission
It is spread mainly by the fecal-oral route due to
fecal contamination of water supplies or food;
person-to-person transmission is uncommon.
52
Symptoms
ALT IgG anti-HEV
IgM anti-HEV
Virus in stool
0 1 2 3 4 5 6 7 8 9 10 11 12 13
Hepatitis E Virus Infection
Typical Serologic Course
Titer
Weeks after Exposure
Diagnosis
ELISA kits are available for IgG and IgM antibodies, using
recombinant and synthetic peptide antigens.
Prevention
Sanitation:
Avoid drinking water of unknown purity, uncooked shellfish,
and uncooked fruit/vegetables not peeled or prepared by
traveler.
Hepatitis G
 GB virus C (GBV-C), formerly known as hepatitis G
virus (HGV) and also known as HPgV is a virus in
the Flaviviridae family and a member of the Pegivirus
genus, is known to infect humans, but is not known to
cause human disease.
 HGV RNA has been found in patients with acute, chronic
and fulminant hepatitis, hemophiliacs, patients with
multiple transfusions and hemodialysis, intravenous drug
addicts and blood donors.
Thank You

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Viral hepatitis

  • 1. Presented By:- Himanshu Dev DMLT VI th Sem. VMMC & SJH
  • 2. What is Viral Hepatitis?  Viral hepatitis is a systemic disease with primary inflammation of the liver by any one of a heterogeneous group of hepatotropic viruses.  The most common causes of viral hepatitis are the five unrelated hepatotropic viruses Hepatitis A, Hepatitis B, Hepatitis C, Hepatitis D, and Hepatitis E.  In addition to the nominal hepatitis viruses, other viruses that can also cause liver inflammation include Herpes simplex, Cytomegalovirus, Epstein–Barr virus, or Yellow fever.
  • 3.  Clinical Terms  Hepatitis: inflammation of liver;  Acute Viral Hepatitis: symptoms last less than 6 months  Acute Hepatic Failure:is the appearance of severe complications rapidly after the first signs of liver disease (such as jaundice), and indicates that the liver has sustained severe damage (loss of function of 80-90% of liver cells).Massive hepatic necrosis with impaired consciousness within 8 weeks of onset of illness.  Chronic Hepatitis: Inflammation of liver for at least 6 months  Cirrhosis: Replacement of liver tissue fibrosis(scar tissue).These changes lead to loss of liver function.  Fulminant Hepatitis: severe impairment of hepatic functions or severe necrosis of hepatocytes in the absence of preexisting liver disease.
  • 4. Viral Hepatitis- Historical Perspective A“Infectious” “Serum” Viral hepatitis Enterically transmitted Parenterally transmitted G E NANB B D C
  • 5.  Types Of Viral Hepatitis Viral Hepatitis A Viral Hepatitis B Viral Hepatitis C Viral Hepatitis D Viral Hepatitis E Agent Hepatitis A virus (HAV); ssRNA; No envelope Hepatitis B virus (HBV); dsDNA; envelope Hepatitis C virus (HCV); ssRNA; envelope Hepatitis D virus (HDV); ssRNA; envelope from HBV Hepatitis E virus (HEV); ssRNA; no envelope Route of Transmission Fecal-oral Parenteral, Vertical, Sexual. Parenteral Parenteral Fecal-oral Age affected Children Any age Adults Any age Young adults Carrier state Nil Common Present Nil (only with HBV) Nil Incubation period 10-50 days (avg. 25-30) 50-180 days (avg. 60-90) 40-120 days 2-12 weeks 2-9 weeks Chronic infection No Yes Yes Yes No Specific Prophylaxis Ig and Vaccine Ig and Vaccine Nil HBV vaccine Nil
  • 6.
  • 7. Hepatitis A  Hepatitis A (formerly known as ―infectious‖ hepatitis or epidemic jaundice) is an acute infectious disease caused by Hepatitis A virus (HAV).  The disease is heralded by non-specific symptoms such as fever, chills, headache, fatigue, generalized weakness and aches and pains, followed by anorexia, nausea, vomiting, dark urine and jaundice.  The disease is benign with complete recovery in several weeks.
  • 8.  Epidemiological determinants Agent factors a) AGENT: The causative agent, the hepatitis A virus, is an enterovirus of the Picornaviridae family. It multiplies only in hepatocytes. b) RESISTANCE: The virus is fairly resistant to heat and chemicals. -Withstands heating to 600 C for 1 hr. and is not affected by chlorine in doses usually employed for chlorination. -Formalin is stated to be an effective disinfectant. -The virus is inactivated by ultraviolet rays and by boiling for 5 minutes or autoclaving. RNA Naked RNA virus
  • 9. c) RESERVOIR OF INFECTION: The human cases are the only reservoir of infection. d) PERIOD OF INFECTIVITY : The risk of transmitting HAV is greatest from 2 weeks before to 1 week after the onset of jaundice. e) INFECTIVE MATERIAL : Mainly man’s faeces. f) VIRUS EXCRETION: HAV is excreted in the faeces for about 2 weeks before onset of jaundice and for up to 2 weeks thereafter.
  • 10. Host factors a) AGE: Infection with HAV is more frequent among children than in adults. However, people from all ages may be infected if susceptible. b) SEX: Both sexes are equally susceptible. c) IMMUNITY: Immunity after attack probably lasts for life. Environmental factors  Cases may occur throughout the year.  In India the disease tends to be associated with periods of heavy rainfall.
  • 11. Mode of Transmission Incubation period 10-50 days (usually 25 to 30 days). a) FAECAL-ORAL ROUTE: Major route of transmission. -By contaminated water, food or milk. b) PARENTERAL ROUTE (Rarely): -By blood and blood products or by skin penetration through contaminated needles. c) SEXUAL TRANSMISSION: -May occur mainly among homosexual men because of oral-anal contact.
  • 12. Diagnosis 1. Demonstration of Virus in feces, blood, bile: By: Immunoelectron microscopy 2. Virus Isolation: 3. Detection of Antibody :By ELISA 4. Biochemical tests: i) Alanine aminotransferase (ALT) ii) Bilirubin iii) Protein 5. Molecular Diagnosis : RT PCR of feces
  • 13.
  • 14. Prevention:- -hygienic measures and sanitation -passive immunization(Human Immunoglobulin Gamma globulin given before exposure to virus or early during the incubation period, will prevent or attenuate a clinical illness. -active immunization Several inactivated or live attenuated vaccines against hepatitis A have been developed. Treatment: -nospecific, dietary food and long rest
  • 15.
  • 16. Hepatitis B Hepatitis B (formerly known as ―serum‖ hepatitis) is an acute systemic infection with major pathology in the liver, caused by hepatitis B virus. Transmitted by the Parenteral route. The acute illness causes liver inflammation, vomiting, jaundice, and, rarely, death. Chronic hepatitis B may eventually cause cirrhosis and liver cancer. Hepatitis B is endemic throughout the world, especially in tropical & developing countries.
  • 17. Epidemiology Determinants Agent factor a) AGENT: Hepatitis B Virus (HBV) -It is a complex, 42 nm double-shelled DNA virus originally known as ―Dane Particle‖. -It replicates in liver cell. HBV occurs in 3 morphology form in serum: i. Small spherical particles with an average Diameter of 22nm. ii. Filamentous or Tubules of varying length & of 22 nm diameter. iii. Dane particle. Out of 3 morphology forms, only the Dane particle is considered infectious, other circulating morphology forms are not infectious.
  • 20. b) RESERVOIR OF INFECTION: -Men is the only reservoir of infection which can be spread either from carriers or from cases. c) Infective material: -Contaminated blood is the main source, -Virus has been found in body secretion such as saliva, vaginal secretion & Semen in infected material. d) Resistance: -Readily destroyed by sodium hypochlorite, as is by heat sterilization in an autoclave for 30-60 min. Host factor a) AGE: -Acute hepatitis B 90% resolve by themselves; <1% develop fulminant hepatic failure. -occurs in approx.: Perinatal -1% Childhood -10%(1-5 yr. age) Late infection -30%(>5 yr. age) -Chronic hepatitis B 2-10% progress to chronic state. -occur in approx. Perinatal -95% Childhood -80% After 5 yr. of age -5-10%
  • 21. b) High Risk Group:  People from endemic regions  Babies of mothers with chronic HBV  Intravenous drug abusers  People with multiple sex partners  Hemophiliacs and other patients requiting blood and blood product treatments  Health care personnel who have contact with blood  Patients who are immunocompromised.
  • 22. c) Humoral and cellular response: -HBV has 3 distinct antigen: i. HBsAg, also known as ―Australian antigen, ii. HBcAg antigen (core antigen) iii. HBeAg envelope antigen They stimulate production of corresponding antibody. Incubation Period 45-180 days (usually 60-90 days)
  • 23. Mode of Transmission  Parenteral- IV drug abusers, health workers are at increased risk.  Sexual- sex workers and homosexuals are particular at risk.  Perinatal (Vertical) – mother (HBeAg+) →infant. Mothers who are HBeAg positive are much more likely to transmit to their offspring than those who are not. Perinatal transmission is the main means of transmission in high prevalence populations.
  • 24. Diagnosis  Serology  Liver Chemistry tests AST, ALT, ALP, and total Bilirubin  Histology--Immunoperoxidase staining  HBV Viral DNA--Most accurate marker of viral DNA and detected by PCR  Liver Biopsy--to determine grade(Inflammation) and stage(Fibrosis) in chronic Hepatitis
  • 25. 1) HBsAg :- It is the first marker to appear in blood after infection. 2) Anti-HBs(HBsAb) :-Disappearance of HBsAg and the appearance of anti-HBs signals recovery from HBV infection, non-infectivity. 3) Anti-HBc :- IgM anti-HBc appears shortly after HBsAg is detect (HBcAg alone dose not appear in serum) IgM-HBc may also or can persist for 3-6 months or longer. IgG-HBc also appear during acute hepatitis B but persist indefinitely. 4) HBeAg :- HBeAg appear in blood concurrently with HBsAg, or soon afterwards. HBeAg is a soluble protein found only in HBeAg positive serum. HBeAg indicate viral replication and infectivity. Persistence of HBeAg in serum beyond 3 month indicate an increased like hood of chronic hepatitis B. Serologic Events
  • 27. Virus/Antibody markers Interpretation HBsAg HBeAg Anti-HBc Anti-HBs Anti-HBe + + IgM - - Acute HBV infection; highly infectious + + IgG - - Late/Chronic HBV infection or carrier state; highly infectivity + - IgG - +/- Late/Chronic HBV infection or carrier state; low infectivity - +/- IgM - +/- Seen rarely in early acute HBV infection; infectious - - IgG +/- +/- Remote HBV infection; infectivity nil or very low - - - + - Immunity following HBV vaccine Interpretation of common serological patterns in HBV infection
  • 28. Prevention  Vaccination - highly effective recombinant vaccines  Hepatitis B Immunoglobulin (HBIG) -exposed within 48 hours of the incident/ neonates whose mothers are HBsAg and HBeAg positive.  Other measures -screening of blood donors, blood and body fluid precautions.
  • 29. National Immunization Schedule Vaccine When to Give Dose Route Site Hepatitis B At birth or as soon as possible with in 24 hours. 0.5 ml IM Antero lateral side of mid thigh Hepatitis B 1,2,3 At 6, 10, 14 weeks 0.5 ml IM Antero lateral side of mid thigh
  • 30. Treatment  Interferon Alfa (Intron A) Response rate is 30 to 40%.  Lamivudine (Epivir HBV) (relapse ,drug resistance)  Adefovir dipivoxil (Hepsera)
  • 31.
  • 32. Hepatitis C  Hepatitis C is an infectious disease affecting primarily the liver, caused by the hepatitis C virus (HCV).  The infection is often asymptomatic, but chronic infection can lead to scarring of the liver and ultimately to cirrhosis, which is generally apparent after many years.  It is estimated that 150–200 million people, or ~3% of the world's population, are living with chronic hepatitis C.  HCV infection is prevalent in India too, with an estimated 12.5 million cases.  Overt jaundice is seen in about 5 % of patients only.  The important part in type C hepatitis is the chronic illness.  About 50 to 80 % of patients progress to chronic hepatitis.
  • 33. Hepatitis C Virus  HCV is a 50-60 nm virus with a linear, single stranded RNA genome, enclosed with in a core and surrounded by an envelope, carrying glycoprotein spikes.  It is a member of the Hepacivirus genus in the family Flaviviridae.  The half life of the virus particles in the serum is around 3 hours and may be as short as 45 minutes.  In addition to replicating in the liver the virus can multiply in lymphocytes.
  • 34. Incubation Period 40-120 days Mode of Transmission  Intravenous Drug Use  Healthcare Exposure: Blood Transfusion, transfusion of Blood products, Organ Transplant without HCV screening carry significant risk of infection.  Hemodialysis  Accidental injuries with needles/sharps  Sexual/household exposure to anti-HCV-positive contact  Multiple sex partners  Vertical Transmission: Vertical transmission of hepatitis C from an infected mother to her child
  • 35. Symptoms anti- HCV ALT Normal 0 1 2 3 4 5 6 1 2 3 4 Hepatitis C Virus Infection Typical Serologic Course Titre Months Years Time after Exposure
  • 36. • HCV antibody – ELISA used to diagnose hepatitis C infection. Not useful in the acute phase as it takes at least 4 weeks after infection before antibody appears. • HCV-RNA - various techniques are available e.g. PCR and branched DNA. May be used to diagnose HCV infection in the acute phase. However, its main use is in monitoring the response to antiviral therapy. • HCV-antigen - an EIA for HCV antigen is available. It is used in the same capacity as HCV-RNA tests but is much easier to carry out. Diagnosis
  • 37. Prevention  Only General Prophylaxis, such as blood, tissue, organ screening, is possible.  No specific active or passive immunizing agent is available. Treatment Interferon - may be considered for patients with chronic active hepatitis. The response rate is around 50% but 50% of responders will relapse upon withdrawal of treatment. Ribavirin - there is less experience with ribavirin than interferon. However, recent studies suggest that a combination of interferon and ribavirin is more effective than interferon alone.
  • 38.
  • 39. Hepatitis D  Hepatitis D, also referred to as hepatitis D virus (HDV) and classified as Hepatitis delta virus, is a disease caused by a small circular enveloped RNA virus.  HDV is considered to be a subviral satellite because it can propagate only in the presence of the hepatitis B virus (HBV).
  • 40. Hepatitis D virus VIRION: spherical, 36-38 nm particle with an outer coat composed of the HBsAg surrounding ssRNA genome. Satellite virus : replicates only in the presence of HBV
  • 41. Incubation Period 2-12 weeks Mode of Transmission The primary route of Transmission are believed to be similar to those of HBV, though HDV does not appear to be sexually transmitted disease.
  • 42. Clinical Features  Infection is dependent on HBV replication, as HBV provides an HBsAg envelop for HDV.  Two types of infection are recognisesd, coinfection and superinfection. In Coinfection, delta and HBV are transmitted together at the same time. In Superinfection, delta infection occurs in a person already harbouring HBV.
  • 43. Diagnosis  Delta antigen is primarily expressed in liver cell nuclei, where it can be demonstrated by immunofluorescence.  Anti-delta antibodies appear in serum and can be identified by ELISA. IgM antibody appears 2-3 weeks after infection and is soon replaced by the IgG antibody in acute delta infection.
  • 44. anti-HBs Symptoms ALT Elevated Total anti-HDV IgM anti-HDV HDV RNA HBsAg HBV - HDV Coinfection Typical Serologic Course Titre Time after Exposure
  • 45. Jaundice Symptoms ALT Total anti-HDV IgM anti-HDV HDV RNA HBsAg HBV – HDV Superinfection Typical Serologic Course Time after Exposure Titre
  • 46.  HBV-HDV Coinfection Pre or post exposure prophylaxis to prevent HBV infection. Screening of blood donor for HBsAg.  HBV-HDV Superinfection Education to reduce risk behaviors among persons with chronic HBV infection. Prevention
  • 47.
  • 48. Hepatitis E  Hepatitis E is a viral hepatitis (liver inflammation) caused by infection with a virus called hepatitis E virus (HEV).  Although Hepatitis E often causes an acute and self-limiting infection (in that it usually goes away by itself and the patient recovers) with low mortality rates.  It bears a high risk of developing chronic hepatitis in immunocompromised patients with substantial mortality rates.  Hepatitis E occasionally develops into an acute, severe liver disease, and is fatal in about 2% of all cases.  In pregnant women the disease is more often severe and is associated with a clinical syndrome called fulminant hepatic failure.
  • 49. Signs and Symptoms Acute Infections: The incubation period of hepatitis E varies from 3 to 8 weeks. After a short prodromal phase symptoms lasting from days to weeks follow. They may include jaundice, fatigue and nausea. Viral RNA becomes detectable in stool and blood serum during incubation period. Serum IgM and IgG antibodies against HEV appear just before onset of clinical symptoms. Recovery leads to virus clearance from the blood, while the virus may persist in stool for much longer. Recovery is also marked by disappearance of IgM antibodies and increase of levels of IgG antibodies. Chronic Infections: While usually an acute disease, in immunocompromised subjects— particularly in solid organ transplanted patients—hepatitis E may cause a chronic infection. Occasionally this may cause liver fibrosis and cirrhosis.
  • 50. Hepatitis E virus  HEV is spherical nonenveloped virus, 29-nm to 32 nm in diameter, with a ssRNA genome.  The surface of the virion shows indentation and spikes.  The Virus is very labile.  II has been classified in the genus Herpes virus under the family Caliciviridae. Incubation Period 2-9 weeks Animal Reservoir: Pigs
  • 51. Mode of Transmission It is spread mainly by the fecal-oral route due to fecal contamination of water supplies or food; person-to-person transmission is uncommon.
  • 52. 52 Symptoms ALT IgG anti-HEV IgM anti-HEV Virus in stool 0 1 2 3 4 5 6 7 8 9 10 11 12 13 Hepatitis E Virus Infection Typical Serologic Course Titer Weeks after Exposure
  • 53. Diagnosis ELISA kits are available for IgG and IgM antibodies, using recombinant and synthetic peptide antigens. Prevention Sanitation: Avoid drinking water of unknown purity, uncooked shellfish, and uncooked fruit/vegetables not peeled or prepared by traveler.
  • 54. Hepatitis G  GB virus C (GBV-C), formerly known as hepatitis G virus (HGV) and also known as HPgV is a virus in the Flaviviridae family and a member of the Pegivirus genus, is known to infect humans, but is not known to cause human disease.  HGV RNA has been found in patients with acute, chronic and fulminant hepatitis, hemophiliacs, patients with multiple transfusions and hemodialysis, intravenous drug addicts and blood donors.