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 antigen is a feature specific to the Adenoviridae. The hexon of mammalian adenoviruses contains a cross-reacting group antigen.

Hosts

Canine adenovirus 1 infection is most common in young dogs, but is becoming less so with the implementation of vaccination strategies. Wild and captive foxes may contract the virus leading to fox encephalitis, and wolves, coyotes and bears can also become clinically infected. Subclinical infections can arise in other carnivores.

Transmission

CAV-1 infection occurs by inhalation and ingestion, after shedding in the urine, faecs or respiratory secretions. Transmission my be by direct contact, or by indirect contact and fomites such as handlers or infected surfaces. Following infection, the virus initially replicates in the tonsils and Peyer's patches. A viraemia is produced, and CAV-1 secondarily localises and replicates in the liver and kidneys.

Canine adenovirus 1 is resistant to environmental inactivation, and can survive for days on fomites at room temperature. Inactivation requires the use of phenol, sodium hydroxide or iodine based disinfectants, or steam cleaning.

Clinical Features

Although there is evidence for a high incidence of infection among the non-vaccinated canine population, this is not matched by a similar occurance of clinically detectable infectious hepatitis since many infections are subclinical. In additions to Infectious Canine Hepatitis, CAV-1 has been shown to be involved in several other types of disease. These include encephalopathy ⁴, ocular lesions, neonatal disease⁵, chronic hepatitis⁶, and interstitial nephritis⁷. The virus can be isolated from throat swabs or lungs from some dogs with respiratory disease, and CAV-1 is known to be of importance in Canine Infectious Tracheobronchitis.

Pathology

Subclinical infection with canine adenovirus 1 most typically causes a mild bronchointerstitial pneumonia, although a necrotising bronchiolitis may occur in immunocompromised dogs. This is seen histologcally as necrosis of the bronchiolar and alveolar epithelium, pulmonary oedema and hyperplasia of type II pneumocytes.

In Infectious Canine Hepatitis, canine adenovirus 1 principally causes damage to the endothelium and to hepatic cells. Endothelial damage results in widespread petechial haemorrhages, and hepatic damage may be visualised as an enlarged liver, mottled with areas of necrosis. Microscopically, centrolobular necrosis is seen in the liver, and adenoviral nuclear inclusion bodies may be observed in Kupffer and parencymal cells. Glomerulonephritis and occular pathology are not uncommon findings.

The pathology exhibited in Infectious Canine Tracheobronchitis varies with other contributing organisms and the severity of disease.

References

1. Rubarth, S (1947) An acute virus disease with liver lesions in dogs (heptatitis contagiosa canis). Acta Path Microbiol Scand, Supplement 67
2. Carbasso, VJ et al (1954) Propagation of infectious canine hepatitis virus in tissue culture. Proc Soc Exp Biol Med, 85
3. 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
4. Whittem, JH, and Blood, DC (1949) Heptatitis contagiosa canis (Rubarth) in Australia. Australian Veterinary Journal, 25
5. Wright, NG, and Cornwell, HJC (1968) Viral induced neonatal disease in puppies. Journal of Small Animal Practice, 9
6. Gocke, DJ et al (1970) Chronic hepatitis in the dog: the role of immune factors. J Am Vet Med Ass, 156
7. Wright, NG at all (1971) Canine adenovirus nephritis. Journal of Small Animal Practice, 12
8. Koptopoulos, G and Cornwell, HJC (1981) Canine adenovirusees: a review. The Veterinary Bulletin, 51(3)
9. Carter, GR and Wise, DJ (2005) A Concise Review of Veterinary Virology, International Veterinary Information Service.
10. Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition) Merial