Canine Hepatitis: Canine Adenovirus Type 1
By Dr. Garret Pachtinger, DACVECC
What is Canine Hepatitis?
Canine adenovirus type 1 (CAV-1) is a nonenveloped DNA virus responsible for infectious canine hepatitis (ICH). CAV–1 recognizes vascular endothelial cells and hepatic (liver) and renal (kidney) cells, resulting in variable disease including liver (hepatic) injury. CAV–2 is antigenically related to CAV-1, but does not cause the same disease. CAV–2 results in respiratory disease in dogs (one of the causes of infectious canine tracheobronchitis).
Signs of Disease
Early in the infection, patients will present with vague clinical signs including loss of appetite, lethargy, vomiting, diarrhea, conjunctivitis, serous discharge from the eyes and nose and notably fever. Patients with more advanced or serious clinical disease may progress to disseminated intravascular coagulation (DIC) as a result of vascular endothelial compromise. Bleeding tendencies seen with DIC may be worsened by liver failure and lack of replacement of consumed clotting factors. Central nervous system signs (hypersalivation, ataxia, seizures) are uncommon but thought to result from vascular damage in the CNS. Corneal opacity (“blue eye”) and interstitial nephritis may occur 1-3 weeks after recovery due to deposition of immune complexes in these organs.
Transmission / Incubation
Oronasal exposure is the most common route of infection resulting from ingestion of urine, feces or saliva of infected dogs. The incubation period is 4–9 days following exposure. Recovered dogs shed virus in their urine for potentially 6 months or longer. Viral spread can also occur via fomites such as food bowls and clothes, and hands of people. Ectoparasites can harbor CAV–1 and may be involved in natural transmission of the disease.
A tentative diagnosis is based on the history, supportive clinical signs and changes in laboratory tests consistent with this infection. Laboratory test changes may include elevation of bloodwork values associated with the liver and kidney, coagulation system disease with abnormalities in PT, PTT, and platelet counts, and CBC changes showing neutrophilia and lymphocytosis. Definitive antemortem diagnosis can be made via commercially available ELISA, serologic and PCR testing. PCR or restriction fragment length polymorphism is required to definitively distinguish CAV–1 from CAV–2. Postmortem evaluation can also be confirmed by virus isolation, immunofluorescence, characteristic intranuclear inclusion bodies in the liver or PCR studies of infected tissue.
The mortality rate ranges from 10%–30%, highest in very young dogs. Concurrent parvoviral or distemper infection worsens the prognosis.
Treatment is symptomatic and supportive. Treatment may include:
- Fluid therapy to correct fluid deficits as a result of lack of intake or gastrointestinal losses (vomiting and diarrhea) and maintenance fluid requirements
- Electrolyte supplementation (e.g. Potassium and magnesium) due to either lack of intake or gastrointestinal losses
- Broad spectrum antibiotic therapy to prevent or treat secondary infection (e.g. aspiration pneumonia)
- Administration of fresh frozen plasma for replacement of clotting factors for patients in liver failure with increased hemorrhagic tendencies
- Nutritional support, either enteral if tolerated or intravenous nutrition if oral feeding is not tolerated by the patient.
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- Overview of Infectious Canine Hepatitis. Merck Veterinary Manual 2008
- Watson PJ: Chronic hepatitis in dogs: a review of current understanding of the etiology, progression, and treatment. Vet J 2004 Vol 167 (3) pp. 228-41.