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H YDROPERICARDIUM
SYNDROME
INCLUSION BODY
HEPATITIS,
A N G A R A D I S E A S E , L I T C H I H E A R T
D I S E A S E
S U M E E T J Y O T I
B V S C & A H
I A A S , T U
INTRODUCTION
Inclusion body hepatitis (IBH) is an adenovirus infection of
poultry characterized by an accumulation of clear, straw-
coloured fluid in the pericardial sac , discoloured liver and
enlarged kidneys, accompanied by intranuclear inclusion
bodies in hepatocytes.
BACKGROUND
• First occurrence was reported in Angara Goth of Karachi (Pakistan)
in August 1987(Khawaja et al.)
• In India, disease was first noticed in the broilers of Jammukashmir
in April 1994.
• On the American continents, the disease was reported in Mexico,
Peru, Ecuador and Chile
• Spread of the disease was also reported in Iraq
BACKGROUND CONTD……
• In Japan, the first outbreak of HPS occurred in 1996,
• In Nepal, this disease was first encountered at Gamcha and Gundu
areas of Bhaktapur district in November 2002.
• Later it spread to Lalitpur, Kabhre, Nuwakot and Dhading districts
of central Nepal
EMERGENCE OF
“HYDROPERICARDIUM
SYNDROME” IN BROILERS OF
NEPAL• In the month of June and July 2009, the veterinarians of Chitwan
had experienced an emergence of Hydropericardium Syndrome
(Singh Subir 2009) in Broilers. In accordance with the research,
disease has showed high spread rate with high morbidity and
mortality pattern. The disease has been reported from
Nawalparashi, Chitwan and Makwanpur
• The cases recorded at VTH (IAAS) Rampur, NAL, Bharatpur and by
several field veterinarians reveals that the disease is in increasing
trend.SPORADIC CASES has been reported in Central veterinary
Laboratory Kathmandu.
ETIOLOGY
• Caused by a disease-producing Group I
(Aviadenovirus) adenovirus
• It is a double stranded DNA virus measuring
about 70-75 nm in diameter.
• There are 12 different serotypes of avian
adenovirus, among them serotype 4 and
serotype 8 are most prevalent. FOWL Adenovirus
SUSCEPTIBLE HOST
• Mainly broiler birds of 3-6 weeks of age.
• Sporadic occurrences of the syndrome have also been reported among
broiler breeders, commercial layer flocks and pigeons.
TRANSMISSION
• Transmission occurs both vertically (egg transmission) and
horizontally (laterally).
• Horizontal spread of virus by latent carriers may be an important
method of spread among flocks on multi-age farms
• Lack of biosecurity, closeness of multi-age farms, and live-bird
trading increase spread of viral agents.
TRANSMISSION CONTD….
• Faecal contamination of clothes, footwear and equipment including
transport crates and vehicles may spread infection
• Contaminated vaccine in some case may act as a source of infection.
• In addition, virus grows in the nasal and tracheal mucosa, conjunctiva and
kidneys, and therefore virus could be present in other secretions or
excretions (OIE,2000)
MORBIDITY AND MORTALITY
• Morbidity rate of inclusion body hepatitis ranges from 10-30 %
• Mortality rate in various outbreaks range between 5% and 10%, but
can reach 30%(OIE) . Typically mortality begins at 3 weeks of age,
peaks in 4th and 5th week and is decreased.
PATHOGENESIS
CHICKENS ONCE AFFECTED BECOMES LIFE LONG CARRIER
AFFECTED ORGAN SHOW LESIONS AT VARIOUS DEGREE.
•VIRUS CAN BE READILY ISOLATED FROM FECES, OCULAR
AND NASAL MUCOSA, BURSA
VIRAEMIA OCCURS WITH SPREADING OF VIRUS TO MANY
ORGANS LIKE LIVER, KIDNEY, RESPIRATORY TRACT, BONE
MARROW AND BURSA.
INITIAL MULTIPLICATION OCCURS IN SMALL AND LARGE
INTESTINE.
VIRUS ENTERS TO THE BODY VIA VARIOUS ROUTES.
CLINICAL FINDINGS
• In natural outbreaks of HPS, the affected birds may not exhibit any
clinical signs other than sudden heavy mortality
• Sudden onset of mortality, dullness, mucoid dropping and crowding
with ruffled feathers are some of the
exhibited signs of the disease.
• Decreased albumin level due to liver
damage.
• About 4-6 hours before death, animals
become reluctant to move, debilitated
and lethargic until death.
LESIONS
• Most prominent gross lesion is excessive
accumulation of clear watery/ jelly like,
straw/ amber or green colored fluid in the
pericardial sac
• Pericardium appears transparent and
occasionally cloudy
• Presence of about 3- 20 ml of fluid in the
pericardial sac.
Straw colored fluid in the pericardial
sac
LESIONS
• Pericardial fat may exhibit yellowish discolouration and petechial
hemorrhages
• Heart appears flabby and its cone is found floating in the pericardial
sac.
• Liver is swollen, pale, friable/mottled and contains large areas of
focal necrotic patches. Occasionally petechiae and echymotic
hemorrhages are found in the liver .
• Kidneys are pale yellow, swollen and friable and contain urate
deposits in the tubules and ureters .
• Lungs are enlarged, congested and edematous with frothy air
passages.
Necrotic focal patches in the liver Swollen liver
DIAGNOSIS
• On the basis of signs and symptoms.(poor diagnostic approach)
• Post mortem lesions
• Histological investigations and detection of intra-nuclear inclusion
bodies in hepatocytes
• Detection of the antigen or virus particles using
immunofluorescence test or electron microscopy
• Isolation and identification of virus by infecting embryonic chick
liver cells.
DIAGNOSIS
• ELISA
• Agar Gel diffusion
• Immunoelectrophoresis
• PCR
TREATMENT
• There is no specific treatment of this disease
• Antibiotics are used to prevent the secondary bacterial infection.
• Iodophore in drinking water (2.5 %) Vegad,J.L, somehow reduces the
mortality .
CONTROL
• It is strictly important to maintain biosecurity to control this disease.
• Breeder flocks should be at least 2 km away from commercial farms.
• Killed or inactivated vaccines should be given which is supposed to
provide 80% protection against the disease.
S
n
TRADE NAME AND CO. COMPOSITION INDICATIONS DOSAGE/ADMIN
ISTRATION
REGIMEN
1. H P VAX (KILLED VACCINE) Oil based
emulsion of
inactivated
suspension of
hepatic tissue of
infected bird
For the protection
of broiler chicks
against HPS
Inject 0.2 ml/bird
by s/c route
7 day old chick
2. NOBILIS FAV (KILLED
VACCINE)
Inactivated
vaccine containing
fowl adenovirus 4
For the protection
against HPS
In broilers,layers
and breeders:
inject o.5 ml by s/c
or i/m
broilers:8-15 days
of age
Layers:16-22
weeks but not less
than 4 weeks
before the onset of
lay
Breeders: at the
age of 8-10 weeks
and second dose
at 16-18 weeks of
age
3. IBH vaccine Inactivated
vaccine
For the protection
against HPS
Chicks: 0.2 ml s/c
Parents: 0.5 ml s/c
route
Chicks: up to 4
weeks
Parents:
THANK YOU!!!

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Hydropericardium syndrome(inclusion body hepatitis)

  • 1. H YDROPERICARDIUM SYNDROME INCLUSION BODY HEPATITIS, A N G A R A D I S E A S E , L I T C H I H E A R T D I S E A S E S U M E E T J Y O T I B V S C & A H I A A S , T U
  • 2. INTRODUCTION Inclusion body hepatitis (IBH) is an adenovirus infection of poultry characterized by an accumulation of clear, straw- coloured fluid in the pericardial sac , discoloured liver and enlarged kidneys, accompanied by intranuclear inclusion bodies in hepatocytes.
  • 3. BACKGROUND • First occurrence was reported in Angara Goth of Karachi (Pakistan) in August 1987(Khawaja et al.) • In India, disease was first noticed in the broilers of Jammukashmir in April 1994. • On the American continents, the disease was reported in Mexico, Peru, Ecuador and Chile • Spread of the disease was also reported in Iraq
  • 4. BACKGROUND CONTD…… • In Japan, the first outbreak of HPS occurred in 1996, • In Nepal, this disease was first encountered at Gamcha and Gundu areas of Bhaktapur district in November 2002. • Later it spread to Lalitpur, Kabhre, Nuwakot and Dhading districts of central Nepal
  • 5. EMERGENCE OF “HYDROPERICARDIUM SYNDROME” IN BROILERS OF NEPAL• In the month of June and July 2009, the veterinarians of Chitwan had experienced an emergence of Hydropericardium Syndrome (Singh Subir 2009) in Broilers. In accordance with the research, disease has showed high spread rate with high morbidity and mortality pattern. The disease has been reported from Nawalparashi, Chitwan and Makwanpur • The cases recorded at VTH (IAAS) Rampur, NAL, Bharatpur and by several field veterinarians reveals that the disease is in increasing trend.SPORADIC CASES has been reported in Central veterinary Laboratory Kathmandu.
  • 6. ETIOLOGY • Caused by a disease-producing Group I (Aviadenovirus) adenovirus • It is a double stranded DNA virus measuring about 70-75 nm in diameter. • There are 12 different serotypes of avian adenovirus, among them serotype 4 and serotype 8 are most prevalent. FOWL Adenovirus
  • 7. SUSCEPTIBLE HOST • Mainly broiler birds of 3-6 weeks of age. • Sporadic occurrences of the syndrome have also been reported among broiler breeders, commercial layer flocks and pigeons.
  • 8. TRANSMISSION • Transmission occurs both vertically (egg transmission) and horizontally (laterally). • Horizontal spread of virus by latent carriers may be an important method of spread among flocks on multi-age farms • Lack of biosecurity, closeness of multi-age farms, and live-bird trading increase spread of viral agents.
  • 9. TRANSMISSION CONTD…. • Faecal contamination of clothes, footwear and equipment including transport crates and vehicles may spread infection • Contaminated vaccine in some case may act as a source of infection. • In addition, virus grows in the nasal and tracheal mucosa, conjunctiva and kidneys, and therefore virus could be present in other secretions or excretions (OIE,2000)
  • 10. MORBIDITY AND MORTALITY • Morbidity rate of inclusion body hepatitis ranges from 10-30 % • Mortality rate in various outbreaks range between 5% and 10%, but can reach 30%(OIE) . Typically mortality begins at 3 weeks of age, peaks in 4th and 5th week and is decreased.
  • 11. PATHOGENESIS CHICKENS ONCE AFFECTED BECOMES LIFE LONG CARRIER AFFECTED ORGAN SHOW LESIONS AT VARIOUS DEGREE. •VIRUS CAN BE READILY ISOLATED FROM FECES, OCULAR AND NASAL MUCOSA, BURSA VIRAEMIA OCCURS WITH SPREADING OF VIRUS TO MANY ORGANS LIKE LIVER, KIDNEY, RESPIRATORY TRACT, BONE MARROW AND BURSA. INITIAL MULTIPLICATION OCCURS IN SMALL AND LARGE INTESTINE. VIRUS ENTERS TO THE BODY VIA VARIOUS ROUTES.
  • 12. CLINICAL FINDINGS • In natural outbreaks of HPS, the affected birds may not exhibit any clinical signs other than sudden heavy mortality • Sudden onset of mortality, dullness, mucoid dropping and crowding with ruffled feathers are some of the exhibited signs of the disease. • Decreased albumin level due to liver damage. • About 4-6 hours before death, animals become reluctant to move, debilitated and lethargic until death.
  • 13. LESIONS • Most prominent gross lesion is excessive accumulation of clear watery/ jelly like, straw/ amber or green colored fluid in the pericardial sac • Pericardium appears transparent and occasionally cloudy • Presence of about 3- 20 ml of fluid in the pericardial sac. Straw colored fluid in the pericardial sac
  • 14. LESIONS • Pericardial fat may exhibit yellowish discolouration and petechial hemorrhages • Heart appears flabby and its cone is found floating in the pericardial sac. • Liver is swollen, pale, friable/mottled and contains large areas of focal necrotic patches. Occasionally petechiae and echymotic hemorrhages are found in the liver . • Kidneys are pale yellow, swollen and friable and contain urate deposits in the tubules and ureters . • Lungs are enlarged, congested and edematous with frothy air passages.
  • 15. Necrotic focal patches in the liver Swollen liver
  • 16.
  • 17. DIAGNOSIS • On the basis of signs and symptoms.(poor diagnostic approach) • Post mortem lesions • Histological investigations and detection of intra-nuclear inclusion bodies in hepatocytes • Detection of the antigen or virus particles using immunofluorescence test or electron microscopy • Isolation and identification of virus by infecting embryonic chick liver cells.
  • 18. DIAGNOSIS • ELISA • Agar Gel diffusion • Immunoelectrophoresis • PCR
  • 19. TREATMENT • There is no specific treatment of this disease • Antibiotics are used to prevent the secondary bacterial infection. • Iodophore in drinking water (2.5 %) Vegad,J.L, somehow reduces the mortality .
  • 20. CONTROL • It is strictly important to maintain biosecurity to control this disease. • Breeder flocks should be at least 2 km away from commercial farms. • Killed or inactivated vaccines should be given which is supposed to provide 80% protection against the disease.
  • 21. S n TRADE NAME AND CO. COMPOSITION INDICATIONS DOSAGE/ADMIN ISTRATION REGIMEN 1. H P VAX (KILLED VACCINE) Oil based emulsion of inactivated suspension of hepatic tissue of infected bird For the protection of broiler chicks against HPS Inject 0.2 ml/bird by s/c route 7 day old chick 2. NOBILIS FAV (KILLED VACCINE) Inactivated vaccine containing fowl adenovirus 4 For the protection against HPS In broilers,layers and breeders: inject o.5 ml by s/c or i/m broilers:8-15 days of age Layers:16-22 weeks but not less than 4 weeks before the onset of lay Breeders: at the age of 8-10 weeks and second dose at 16-18 weeks of age 3. IBH vaccine Inactivated vaccine For the protection against HPS Chicks: 0.2 ml s/c Parents: 0.5 ml s/c route Chicks: up to 4 weeks Parents: