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Year : 2006, Volume : 30, Issue : 1
First page : ( 53) Last page : ( 54)
Print ISSN : 0250-4758. Online ISSN : 0973-970X. Published online : 2006 June 1.

Pathogenesis of inclusion body hepatitis (IBH) virus in experimentally infected broiler chicks and chick embryos*

Kumar Prabhat1,3Research Associate, Singh Surendra3, Singh S.D.2,3Principal Scientists, Jaiswal T.N.3Ex-Emeritus Scientist

3Centre for Studies in MicrobiologyJiwaji University, Gwalior-474 011(MP)

1B&M Div., IVRI, Izatnagar,

2IVRI, Izatnagar

*Part of the PhD thesis submitted by the first author to JU Gwalior;

Clinical signs and mortality

Experimentally infected chicks with IBH virus were found dull, depressed and sitting aside with closed eyes. There were loss of feed intake, ruffled feathers and greenish-white faeces at later stages. After 2–3 days of post-inoculation, the chicks started dying and within 7 days period, mortality was found up to 80%. Chicks in control group did not reveal any clinical signs, lesions or mortality. In chick embryos inoculated with IBH virus, mortality started after 3rd day of infection and the mortality up to 100% was observed. Severe haemorrhages in head, neck and legs were recorded. Similar observations, i.e., severe haemorrhages and 100% mortality in chick embryos were reported6.

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Gross lesions

The dead and sacrificed chicks were necropsied. The gross lesions recorded were characteristic hydropericardium in heart in dead and sacrificed chicks during 3–6 days post-infection. Accumulation of straw-coloured watery fluid was observed in pericardial sac (Fig. 1). No such lesions were observed in the heart of chicks of uninoculated control group. Liver was found enlarged and dark-red coloured with multiple pin-point necrotic foci. In unincoulated control group, the liver was normal without any such gross lesions. Similar gross lesions have been observed by earlier workers in naturally infected chick with IBH- HPS virus1, 2. Spleen was found slightly congested in chicks of virus-inoculated group. Kidneys were swollen, congested and pale in majority of cases as compared to that of uninoculated control group.

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Histopathological lesions

The liver, heart, spleen, kidneys and trachea from infected as well as control groups were examined for histopathological changes. Liver revealed congestion of blood vessels and haemorrahges with engorged and dilated hepatic sinusoids. There were degeneration of hepatic cells and focal areas of necrosis along with disorganization of hepatic lobules. Mild degenerative changes were seen through- out the parenchyma. Inflammatory changes consisted of necrosis, degeneration and infiltration of heterophills and lymphocytes. Large, round basophilic intranuclear inclusion bodies were seen in hepatocytes during early phase of infection (Fig.2). These findings were similar in characteristics as reported by earlier workers2, 6, 9. Bile duct hyperplasia and fibroblastic tissue proliferation were also seen at later stages (Fig.3). Spleen showed focal areas of necrosis and depletion of splenocytes and in later stages, there were formation of secondary lymphoid nodules. Trachea revealed haemorrhages, lymphoid aggregations, hyperactivation of epithelial cells and glandular hypertrophy in chicks, which were found alive after infection. IBH virus, being an immunosuppressive in nature, might have caused immunosuppression in infected chicks and thereby causing secondary bacterial and mycoplasmal infections in respiratory tract, leading to pathological changes in trachea.

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Figures

Fig. 1::

Hydropericardium and enlarged liver covered with fibrinous layer in IBH virus infected chick




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Fig. 2::

Section of liver, showing basophilic intranuclear inclusion bodies in hepatocytes. HE × 700




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Fig. 3::

Section of liver, showing bile duct hyperplasia and fibrous tissue proliferation. HE × 100



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