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Hydropericardium in poultry

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This document discusses hydropericardium syndrome, a disease affecting broiler chickens caused by group I adenovirus. The disease is characterized by an accumulation of fluid under the pericardium and liver necrosis. It is transmitted both vertically from breeders and horizontally. The virus infects the intestines then spreads systemically, being shed in feces. Affected chickens show sudden high mortality between 3-5 weeks with lethargy and yellow droppings. Necropsy reveals fluid in the pericardium and pale swollen liver and kidneys. Histopathology shows liver and heart lesions and inclusion bodies aid diagnosis along with PCR and immunofluorescence tests.

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Hydropericardium in poultry
INTRODUCTION Also known as Hydropericardiumhepatitis syndrome leechi disease or angara disease The disease occurs usually in 3-5 week-old healthy broilers . Characterized by high morbidity and mortality, excess accumulation of fluid under pericardium and many areas of necrotic foci in the liver
ETIOLOGY Caused by group I adenovirus ( mostly serotype 4 & 8) The adenovirus is a non-enveloped icosahedral, The nucleic acid is linear, ds DNA These viruses are capable of producing the disease without the immunosuppressive effects of associated viruses such as IBD or other immunosuppressive agents.
Transmission It is transmitted both vertically and horizontally Adenovirus may remain latent in breeding stock until the onset of maturity and then are shed following immunosuppression or stress Horizontal spread of virus by carriers occurs. Fecal contamination of clothes, footwear and equipment including transport crates and vehicles may spread infection.
PATHOGENESIS VIRUS ENTERS INTO THE BODY INITIAL MULTIPLICATION OF THE VIRUS OCCURS IN SMALL AND LARGE INTESTINE. VIRAEMIA OCCURS WITH SPREADING OF VIRUS TO MANY ORGANS LIKE LIVER, KIDNEY, RESPIRATORY TRACT, BONE MARROW AND BURSA. VIRUS CAN BE READILY ISOLATED FROM FECES, OCULAR AND NASAL MUCOSA, BURSA
Chicken once affected with adenovirus becomes lifelong carrier.
SIGNS AND SYMPTOMS Sudden increase in mortality (20-80%): Mortality starts at about 3 weeks and reaches its peak in 4 to 5 weeks. flocks of 3-5 weeks old broilers with HP may not show specific signs i.e. bird may remain active just until before death, but abrupt onset of mortality with lethargy, ruffled feather & yellow mucoid dropping may be seen
Hydropericardium in poultry
Gross lesions Straw coloured clear, jelly like fluid upto 20 ml in pericardial sac i.e. hydropericardium Enlarged pale friable liver The kidneys are pale, swollen and mottled appearance accumulation of fluid in lungs. Generalized congestion
Hydropericardium in poultry
Hydropericardium in poultry
Hydropericardium in poultry
Histopathological lesions Myocardial edema in heart with degeneration, necrosis and mononuclear cell infiltration Basophilic intranuclear inclusion bodies may be present in liver In many of the hepatic cells, the nuclei disappear entirely, leaving a ghost cell consisting of one or more large vacuoles.
Hydropericardium in poultry
Hydropericardium in poultry
Diagnosis Necropsy: gross and microscopic lesion histological investigations and detection of intra-nuclear inclusion bodies in hepatocytes detection of the antigen or virus particles using immunofluorescence test or electron microscopy PCR

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Hydropericardium in poultry

  • 2. INTRODUCTION Also known as Hydropericardiumhepatitis syndrome leechi disease or angara disease The disease occurs usually in 3-5 week-old healthy broilers . Characterized by high morbidity and mortality, excess accumulation of fluid under pericardium and many areas of necrotic foci in the liver
  • 3. ETIOLOGY Caused by group I adenovirus ( mostly serotype 4 & 8) The adenovirus is a non-enveloped icosahedral, The nucleic acid is linear, ds DNA These viruses are capable of producing the disease without the immunosuppressive effects of associated viruses such as IBD or other immunosuppressive agents.
  • 4. Transmission It is transmitted both vertically and horizontally Adenovirus may remain latent in breeding stock until the onset of maturity and then are shed following immunosuppression or stress Horizontal spread of virus by carriers occurs. Fecal contamination of clothes, footwear and equipment including transport crates and vehicles may spread infection.
  • 5. PATHOGENESIS VIRUS ENTERS INTO THE BODY INITIAL MULTIPLICATION OF THE VIRUS OCCURS IN SMALL AND LARGE INTESTINE. VIRAEMIA OCCURS WITH SPREADING OF VIRUS TO MANY ORGANS LIKE LIVER, KIDNEY, RESPIRATORY TRACT, BONE MARROW AND BURSA. VIRUS CAN BE READILY ISOLATED FROM FECES, OCULAR AND NASAL MUCOSA, BURSA
  • 6. Chicken once affected with adenovirus becomes lifelong carrier.
  • 7. SIGNS AND SYMPTOMS Sudden increase in mortality (20-80%): Mortality starts at about 3 weeks and reaches its peak in 4 to 5 weeks. flocks of 3-5 weeks old broilers with HP may not show specific signs i.e. bird may remain active just until before death, but abrupt onset of mortality with lethargy, ruffled feather & yellow mucoid dropping may be seen
  • 9. Gross lesions Straw coloured clear, jelly like fluid upto 20 ml in pericardial sac i.e. hydropericardium Enlarged pale friable liver The kidneys are pale, swollen and mottled appearance accumulation of fluid in lungs. Generalized congestion
  • 13. Histopathological lesions Myocardial edema in heart with degeneration, necrosis and mononuclear cell infiltration Basophilic intranuclear inclusion bodies may be present in liver In many of the hepatic cells, the nuclei disappear entirely, leaving a ghost cell consisting of one or more large vacuoles.
  • 16. Diagnosis Necropsy: gross and microscopic lesion histological investigations and detection of intra-nuclear inclusion bodies in hepatocytes detection of the antigen or virus particles using immunofluorescence test or electron microscopy PCR