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Ahmad Hassan
2020-AG-443
Hepatitis E virus infections in chicken
Contents :
Introduction
Etiology
Morphology
Chemical composition
Transmission
Hepatitis E virus infections in chicken
Contents :
Susceptibility to Chemical
and Physical Agents
Clinical Signs
Gross Lesions
Pathogenesis
Control
Diagnosis
Introduction and history
Hepatitis‐splenomegaly (HS) syndrome is a disease of
layer and broiler‐breeder chickens. First described in Australia in
the 1980s and subsequently in the UK and USA .
Although first described as HS syndrome, the disease is also referred
to as big liver and spleen (BLS) disease,.
Characterized by
increased mortality and decreased egg production and is
caused by avian hepatitis E virus (avian HEV)
Dead birds have red fluid or clotted blood in their abdomens,
and enlarged livers and spleens,
regressed or ruptured ovaries
Etiology
The primary causative agent of HS syndrome or BLS is
avian HEV.
All HEV are classified in the family of Hepeviridae.
The virus genome was sequenced and found to have over 60%
similarity to human Hepatitis E virus. Further studies are
required in order to fully characterize
and determine the classification of the virus
Morphology
Human HEV is a spherical, non‐enveloped, symmetrical
virus particle of approximately 32–34 nm in diameter.
bile samples from chickens with HS
syndrome are almost similar in size and morphology to human
HEV.
Chemical composition
The genome of avian HEV is a single stranded,
positive sense RNA molecule of 6,654 bp in
length excluding the poly (A) tail, which is
approximately 600 bp shorter than that of
mammalian HEVs
Virus spead and transmission
Horizontal transmission occurs between flocks on farms by the
faecal–oral route, although
spread within a flock may be relatively slow.
BLS antigen was detected in 1-day-old culled broiler chicks and
in the livers of broiler chickens that were the progeny of a BLS
affected flock. Thus, suggesting that vertical transmission
probably occurs following field infection. Chickens of all ages
are susceptible to infection but clinical disease is only seen in
birds over 24 weeks of age.
Susceptibility to Chemical
and Physical Agents
Liver suspensions containing avian HEV remained infectious
after treatment with chloroform and ether but
lost infectivity after incubating at 56°C for 1 hour or 37°C
for 6 hours.
Pathogenesis
The gastrointestinal tissues appear to be the first site of
avian HEV replication following oral inoculation,
Avian HEV is thought to enter the host through the fecal–oral
route. After replication in the liver, avian HEV is released to the
gallbladder from hepatocytes and then is excreted in feces.
Clinical Signs
The morbidity and mortality due to the disease in the
field are low, and the majority of avian HEV infections
are subclinical, In some outbreaks, there has been a drop in
egg production of up to 20%, but in other outbreaks egg
production
has not been affected. Hepatitis‐splenomegaly syndrome is
characterized by above‐normal mortality in broiler
breeder hens and laying hens of 30–72 weeks of age.
Gross lesions
At postmortem examination,birds are generally in good bodily condition
but there are gross changes to the liver, spleen and ovaries.
Liver : The liver is often enlarged and small subcapsular haemorrhages
are seen.
Red fluid in the abdomen may be present with clotted blood.
Spleen: The spleen is two or three times larger than normal with a mottled
appearance ,
blood can be seen in the abdominal cavity
Ovaries : Regression and rupture of the ovaries may occur, causing egg
peritonitis. Other lesions include pulmonary congestion with oedema and
enteritis, particularly in the duodenum.
.
Enlarged and haemorrhagic liver
from a chicken with
hepatitis‐splenomegaly syndrome
(HSS)
.
Two enlarged and
mottled white spleens
from 56‐week‐old
chickens with
hepatitis‐splenomegaly
syndrome
Diagnosis
A presumptive diagnosis of HS syndrome can be made on
the basis of clinical signs and pathological lesions.
However, ELISA and (R-T) PCR are useful in the identification.
Control
A vaccine against avian HEV is not yet available.
Currently there is no treatment for avian HEV infection.
Implementation of strict biosecurity in chicken farms
may limit the spread of virus.
Thank you
.REF : DISEASES OF POULTRY / EDITOR-IN-CHIEF, DAVID E. SWAYNE ;
ASSOCIATE
EDITORS, MARTINE BOULIANNE
POULTRY DISEASES SIXTH EDITION BY MARK EDDISON, PUAL F
MCMULLIN

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Hepatitis E virus infections in chicken

  • 2. Hepatitis E virus infections in chicken Contents : Introduction Etiology Morphology Chemical composition Transmission
  • 3. Hepatitis E virus infections in chicken Contents : Susceptibility to Chemical and Physical Agents Clinical Signs Gross Lesions Pathogenesis Control Diagnosis
  • 4. Introduction and history Hepatitis‐splenomegaly (HS) syndrome is a disease of layer and broiler‐breeder chickens. First described in Australia in the 1980s and subsequently in the UK and USA . Although first described as HS syndrome, the disease is also referred to as big liver and spleen (BLS) disease,.
  • 5. Characterized by increased mortality and decreased egg production and is caused by avian hepatitis E virus (avian HEV) Dead birds have red fluid or clotted blood in their abdomens, and enlarged livers and spleens, regressed or ruptured ovaries
  • 6. Etiology The primary causative agent of HS syndrome or BLS is avian HEV. All HEV are classified in the family of Hepeviridae. The virus genome was sequenced and found to have over 60% similarity to human Hepatitis E virus. Further studies are required in order to fully characterize and determine the classification of the virus
  • 7. Morphology Human HEV is a spherical, non‐enveloped, symmetrical virus particle of approximately 32–34 nm in diameter. bile samples from chickens with HS syndrome are almost similar in size and morphology to human HEV.
  • 8. Chemical composition The genome of avian HEV is a single stranded, positive sense RNA molecule of 6,654 bp in length excluding the poly (A) tail, which is approximately 600 bp shorter than that of mammalian HEVs
  • 9. Virus spead and transmission Horizontal transmission occurs between flocks on farms by the faecal–oral route, although spread within a flock may be relatively slow. BLS antigen was detected in 1-day-old culled broiler chicks and in the livers of broiler chickens that were the progeny of a BLS affected flock. Thus, suggesting that vertical transmission probably occurs following field infection. Chickens of all ages are susceptible to infection but clinical disease is only seen in birds over 24 weeks of age.
  • 10. Susceptibility to Chemical and Physical Agents Liver suspensions containing avian HEV remained infectious after treatment with chloroform and ether but lost infectivity after incubating at 56°C for 1 hour or 37°C for 6 hours.
  • 11. Pathogenesis The gastrointestinal tissues appear to be the first site of avian HEV replication following oral inoculation, Avian HEV is thought to enter the host through the fecal–oral route. After replication in the liver, avian HEV is released to the gallbladder from hepatocytes and then is excreted in feces.
  • 12. Clinical Signs The morbidity and mortality due to the disease in the field are low, and the majority of avian HEV infections are subclinical, In some outbreaks, there has been a drop in egg production of up to 20%, but in other outbreaks egg production has not been affected. Hepatitis‐splenomegaly syndrome is characterized by above‐normal mortality in broiler breeder hens and laying hens of 30–72 weeks of age.
  • 13. Gross lesions At postmortem examination,birds are generally in good bodily condition but there are gross changes to the liver, spleen and ovaries. Liver : The liver is often enlarged and small subcapsular haemorrhages are seen. Red fluid in the abdomen may be present with clotted blood. Spleen: The spleen is two or three times larger than normal with a mottled appearance , blood can be seen in the abdominal cavity Ovaries : Regression and rupture of the ovaries may occur, causing egg peritonitis. Other lesions include pulmonary congestion with oedema and enteritis, particularly in the duodenum.
  • 14. . Enlarged and haemorrhagic liver from a chicken with hepatitis‐splenomegaly syndrome (HSS)
  • 15. . Two enlarged and mottled white spleens from 56‐week‐old chickens with hepatitis‐splenomegaly syndrome
  • 16. Diagnosis A presumptive diagnosis of HS syndrome can be made on the basis of clinical signs and pathological lesions. However, ELISA and (R-T) PCR are useful in the identification.
  • 17. Control A vaccine against avian HEV is not yet available. Currently there is no treatment for avian HEV infection. Implementation of strict biosecurity in chicken farms may limit the spread of virus.
  • 18. Thank you .REF : DISEASES OF POULTRY / EDITOR-IN-CHIEF, DAVID E. SWAYNE ; ASSOCIATE EDITORS, MARTINE BOULIANNE POULTRY DISEASES SIXTH EDITION BY MARK EDDISON, PUAL F MCMULLIN