Difference between revisions of "Infectious Canine Hepatitis"

Revision as of 11:12, 4 August 2010

Also known as:

Rubarth's Disease
Canine adenovirus infection

Description

Infectious Canine Hepatitis (ICH) is a highly contagious disease of dogs caused by Canine Adenovirus 1 (CAV1). This virus is closely related to Canine Adenovirus 2, which causes respiratory disease.

Canine Adenovirus 1 invades via the oronasal route following excretion in the urine and faeces. Urinary excretion can persist for up to nine months after an active infection, and the virus may also be spread by contaminated fomites. Once established, CAV1 replicates in the cells of the oropharynx before a viraemia causes dissemination to other tissues. A trophism exists for hepatic parenchyma and vascular endothelium: the target organs of CAV1 are therefore the liver, kidney, vascular endothelium and eye.

In the liver, the clinical outcome of CAV1 infection depends on the level of pre-existing immunity. Animals with high antibody titres usually mount an effective neutralising antibody response by day seven post-infection which clears the virus. Outcome is variable when a partial antibody response is mounted four to five days post-infection: both chronic active hepatitis (and ultimately hepatic fibrosis) and latent hepatic infection are possible. Low antibody titres, such as in unvaccinated dogs, fail to prevent infection and pathology and lead to potentially fatal hepatic necrosis. This necrosis is initially widespread and centrilobular, but may progress to become panlobular. In the kidney, virus localisation or deposition of circulating immune complexes causes glomerular damage and thus proteinuria. Immune complexes may also be deposited in the cornea and uveal tract, damaging the eye. In addition to glomerular localisation, CAV persists in the renal tubular epithelium, accounting for the extended period of urinary excretion of virus. The virus may similarly localise to the vascular endothelium, leading to vasculitis and bleeding diatheses.

Immune complex deposition in the cornea and uveal tract causes damage to the eye. Direct cytotoxic damage to the eye may also occur.

Signalment

Young, unvaccinated dogs are most often affected.

Diagnosis

Clinical Signs

Signs may be peracute or acute in onset.

In acute cases, key clinical findings are vomiting, abdominal pain, anorexia, diarrhoea and pyrexia. Signs of a bleeding disorder can be present in some cases. Clinical examination may reveal a combination of many features. These could include: lymphadenopathy, pharyngitis or tonsilar enlargement, pneumonia, abdominal distension and/or pain, hepatomegaly, jaundice, petechial or ecchymotic haemorrhages, epistaxis, bleeding from venipuncture sites or CNS signs such as depression, disorientation and seizures. Clinical signs tend to pesrsist for five to seven days before improvement is noted. During the recovery phase, 20% of cases develop corneal oedema and anterior uveitis ("blue eye").

In peracute cases, death rapidly follows the onset of clinical signs.

Laboratory Tests

Radiography

Biopsy

Endoscopy

Pathology

Gross

The liver is enlarged and friable on post-mortem examination. Extensive centrilobular necrosis leads to a pale, mottled appearance, but widespread haemorrhage is also apparent. These haemorrhages are located particularly on the serosal surface. Ascites results from this hepatitis, and fibrinous or fibrino-haemorrhagic adhesions can sometimes be seen between the lobes of the liver.

Other organs may also show changes. For example, the wall of the gall bladder may be oedematous, and lymph nodes can be enlarged, reddened and haemorrhagic. Chronic interstitial nephritis may feature.

Histological

Histopathology reveals centrilobular necrosis. Haematoxylin and eosin staining reveals basophilic intranuclear inclusion bodies in hepatocytes and macrophages. It is possible to use immunofluorescence to stain for viral antigen in vascular endothelium.

Treatment

Control

In an outbreak

Isolate infected dogs
Disinfect premises

To prevent

Vaccination: tissue culture adaptation that may be live or inactivated
Cross protection with CAV2
Live vaccines are known to cause keratitis in Afghans, Red Setters and Saluki

Prognosis

References

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 ==Description==
 Infectious Canine Hepatitis (ICH) is a highly contagious disease of dogs caused by [[Canine Adenovirus 1]] (CAV1). This virus is closely related to Canine Adenovirus 2, which causes respiratory disease.
-Canine Adenovirus 1 invades via the oronasal route following excretion in the urine and faeces. Urinary excretion can persist for up to nine months after an active infection, and the virus may also be spread by contaminated fomites. Once established, CAV1 replicates in the cells of the oropharynx before a viraemia causes dissemination to other tissues. A trophism exists for hepatic parenchyma and vascular endothelium: the target organs of CAV1 are therefore the liver, vascular endothelium, kidney and eye.
+Canine Adenovirus 1 invades via the oronasal route following excretion in the urine and faeces. Urinary excretion can persist for up to nine months after an active infection, and the virus may also be spread by contaminated fomites. Once established, CAV1 replicates in the cells of the oropharynx before a viraemia causes dissemination to other tissues. A trophism exists for hepatic parenchyma and vascular endothelium: the target organs of CAV1 are therefore the liver, kidney, vascular endothelium and eye.
-In the liver, the clinical outcome of CAV1 infection depends on the level of pre-existing immunity. Animals with high antibody titres usually mount an effective neutralising antibody response by day seven post-infection which clears the virus. Outcome is variable when a partial antibody response is mounted four to five days post-infection: both chronic active hepatitis (and ultimately hepatic fibrosis) and latent hepatic infection are possible. Low antibody titres, such as in unvaccinated dogs, fail to prevent infection and pathology and lead to potentially fatal hepatic necrosis. This necrosis is initially widespread and centrilobular, but may progress to become panlobular.
-Damage caused by localisation to the vascular endothelium can lead to vasculitis and bleeding diatheses such as disseminated intravascular coagulation.
-In the kidney, glomerular damage results from localisation of virus or deposition of circulating immune complexes. This can lead to proteinuia. It is also possible for CAV1 to persist in renal tubular epithelium; this is responsible for the extended period of urinary excretion of virus.
+In the liver, the clinical outcome of CAV1 infection depends on the level of pre-existing immunity. Animals with high antibody titres usually mount an effective neutralising antibody response by day seven post-infection which clears the virus. Outcome is variable when a partial antibody response is mounted four to five days post-infection: both chronic active hepatitis (and ultimately hepatic fibrosis) and latent hepatic infection are possible. Low antibody titres, such as in unvaccinated dogs, fail to prevent infection and pathology and lead to potentially fatal hepatic necrosis. This necrosis is initially widespread and centrilobular, but may progress to become panlobular. In the kidney, virus localisation or deposition of circulating immune complexes causes glomerular damage and thus proteinuria. Immune complexes may also be deposited in the cornea and uveal tract, damaging the eye. In addition to glomerular localisation, CAV persists in the renal tubular epithelium, accounting for the extended period of urinary excretion of virus.  The virus may similarly localise to the vascular endothelium, leading to vasculitis and bleeding diatheses.
 Immune complex deposition in the cornea and uveal tract causes damage to the eye. Direct cytotoxic damage to the eye may also occur.