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.

2. INTRODUCTION
 Also known as “Hydropericardium–hepatitis
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 it’s 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