Difference between revisions of "Infectious Canine Hepatitis"

Revision as of 10:53, 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, vascular endothelium, kidney and eye.

In the liver, widespread centrilobular necrosis occurs, which may progress to become panlobular. The clinical outcome of CAV1 infection is dependent 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. A partial antibody response withing four to five days post-infection can lead to chronic active hepatitis and ultimately hepatic fibrosis. Latent chronic hepatic infection is also possible. Low antibody titres, such as in unvaccinated dogs, fail to prevent infection and pathology, giving potentially fatal hepatic necrosis.

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.

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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 |Rubarth's Disease <BR> 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 may be shed in the urine for up to nine months following an active infection, and is also spread by infected faeces and fomites. After invasion via the oronasal route,
+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.
-CAV1 infects and replicates in the cells of the oropharynx. A viraemia becomes established, which allows dissemination of infection to other tissues. CAV1 has a tropism for hepatic parenchyma and vascular endothelium, and so the key target organs are the liver, vascular endothelium, kidney and eye.
 In the liver, widespread centrilobular necrosis occurs, which may progress to become panlobular. The clinical outcome of CAV1 infection is dependent 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. A partial antibody response withing four to five days post-infection can lead to chronic active hepatitis and ultimately hepatic fibrosis. Latent chronic hepatic infection is also possible. Low antibody titres, such as in unvaccinated dogs, fail to prevent infection and pathology, giving potentially fatal hepatic necrosis.