Canine Adenovirus 1
Introduction
Canine Adenovirus 1 (CAV-1) was first isolated by Carbasso in 19541 from a case of acute hepatitis in the dog. This virus found to be identical to the virus isolated in 1947 by Rubarth2 from a dog showing acute liver lesions, and so CAV-1 was originally known as Infectious Canine Hepatitis (ICH) virus. Subsequently, CAV1 infection was shown to be common in young dogs worldwide, with 82% of British dogs displaying neutralising antibody titres by nine months of age3. It has also since been demonstrated that CAV1 has a role in diseases other than Infectious Canine Hepatitis, such as Canine Infectious Tracheobronchitis.
Classification
CAV-1 is a member of the Adenoviridae family, a group double-stranded DNA viruses with an icosahedral nucleocapsid. Many Adenoviridae have been isolated from mammals and birds, but only a small number of these cause significant veterinary disease. The family consists of four genera: Mastadenovirus, Aviadenovirus, Atadenovirus and Siadenovirus. Canine adenovirus 1 is a Mastadenovirus.
Viral Characteristics
The genetic information of CAV-1, like other Adenoviridae, is conveyed by a single, linear molecule of double-stranded DNA which encodes around 30 proteins. Under the influence of both host and virus-encoded factors, the DNA replicates and is transcribed within the host nucleus, where virion assembly also occurs. Basophilic and/or acidophilic inclusions may therefore be seen in the nucleus of an adenovirus-infected cell.
The virus genome is contained within a non-enveloped icosohedral nucleocapsid, which comprises capsomeres (called hexons) and twelve vertex capsomeres (called pentons). A fibre antigen protrudes from each of the twelve pentons, and this attaches to host cell receptors as well as being a type-specific haemagglutinin. This fibre antige is a feature specific to the Adenoviridae. The hexon of mammalian adenoviruses contains a cross-reacting group antigen.
Hosts
- Dogs
- Foxes are very susceptible (Fox Encephalitis)
Occurrence Dogs younger than one year of age are most often affected. The virus also infects wild and captive foxes causing encephalitis, and wolves, coyotes and bears. Other carnivores may sustain subclinical infections. The disease occurs commonly worldwide, but is uncommon where vaccination is practiced.
Transmission and Epidemiology
- Transfers easily via ingesting infected urine, feces or respiratory secretions
- Can be transferred by handlers, infected surfaces, etc
Infection is by inhalation and ingestion. Spread is by direct and indirect contact.
The virus replicates initially in tonsils and Peyer’s patches producing a viremia with secondary localization and replication in the liver and kidney
.
Disease
This high incidence of infection is not matched by a similar incidence of clinical hepatitis, and it si now known that many infections are subclinical and that the virus is also responsible for other conditions, e.g. encephalopathy, ocular disease, neonatal disease, chronic hepatitis, and interstitial nephritis. In several countries, the virus has been isolated from throat swabs or lungs from dogs with respiratory disease, and in Britain CAV-1 is thought to be of importane in kennel cough (infectious tracheobronchitis).
Clinical signs include depression, fever, vomiting, diarrhea, and discharges from the nose and eyes. Because of a tendency to bleed, hematomas may be seen in the mouth.
- Adenoviridae
- Usually mild bronchointerstitial pneumonia, necrosis of bronchiolar and alveolar epithelium, oedema, type II pneumocyte hyperplasia
- May cause necrotising bronchiolitis in immune-deficient dogs (distemper)
- Can be associated with kennel cough described ab
The principal tissue changes involve the endothelium and hepatic cells. Damaged endothelium results in widespread petechial hemorrhages. The liver may be enlarged or normal in size, but usually is mottled because of focal areas of necrosis. Microscopically, the most significant changes are found in the liver, where centrolobular necrosis is noted and typical adenoviral inclusion bodies are observed in Kupffer cells and parenchymal cells. Circulating immune complexes in the glomeruli may result in glomerulonephritis. Recovered dogs may develop a transient corneal opacity ("blue eye") as a result of local immune complex deposition. Recovery from infectious canine hepatitis (ICH) results in lasting immunity. Diagnosis Clinical specimens: liver, spleen, kidney, blood, urine, nasal swabs and paired serum samples. Diagnosis of ICH is usually made on the basis of clinical signs and gross and microscopic lesions including the presence of basophilic inclusions in hepatocytes, endothelial cells, and Kupffer cells. The virus can be demonstrated in frozen liver sections by immunofluorescence. The virus can be cultivated in cell cultures of canine origin. The liver has been reported to be less suitable for virus recovery than other vital organs. A rising titer of antibodies employing hemagglutination inhibition or virus neutralization are supportive of a diagnosis. Prevention Modified live and killed vaccines are used, often in combination with parvovirus and canine distemper antigens. Modified live vaccines induce a longer lasting immunity, but a small percentage of vaccinated dogs may develop ocular or renal lesions. These core canine vaccines were traditionally administered annually but are now, depending on the type of vaccine, often given less frequently.
References
- Rubarth, S (1947) An acute virus disease with liver lesions in dogs (heptatitis contagiosa canis). Acta Path Microbiol Scand, Supplement 67
- Carbasso, VJ et al (1954) Propagation of infectious canine hepatitis virus in tissue culture. Proc Soc Exp Biol Med, 85
- Ablett, RE and Baker, LA (1960) The development in the dog of naturally acquired antibody to canine hepatitis in relation to age. The Veterinary Record, 72
- Koptopoulos, G and Cornwell, HJC (1981) Canine adenovirusees: a review. The Veterinary Bulletin, 51(3)
