Difference between revisions of "Canine Adenovirus 1"
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| − | Also known as: '''''CAV-1 | + | |
| + | Also known as: '''''CAV-1 - Infectious Canine Hepatitis Virus - ICH virus''''' | ||
==Introduction== | ==Introduction== | ||
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==Pathology== | ==Pathology== | ||
| − | Subclinical infection with canine adenovirus 1 most typically causes a mild bronchointerstitial pneumonia, although a necrotising bronchiolitis may occur in immunocompromised dogs. Bronchointerstitial pneumonia is seen | + | Subclinical infection with canine adenovirus 1 most typically causes a mild bronchointerstitial pneumonia, although a necrotising bronchiolitis may occur in immunocompromised dogs. Bronchointerstitial pneumonia 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 parenchymal cells. Glomerulonephritis and occular pathology are not uncommon findings. | 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 parenchymal cells. Glomerulonephritis and occular pathology are not uncommon findings. | ||
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The pathology exhibited in [[Infectious Canine Tracheobronchitis]] varies with the other contributing organisms and the severity of disease. | The pathology exhibited in [[Infectious Canine Tracheobronchitis]] varies with the other contributing organisms and the severity of disease. | ||
| − | + | ==Literature Search== | |
| − | | | + | [[File:CABI logo.jpg|left|90px]] |
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| + | Use these links to find recent scientific publications via CAB Abstracts (log in required unless accessing from a subscribing organisation). | ||
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| + | [http://www.cabdirect.org/search.html?rowId=1&options1=AND&q1=%22canine+adenovirus+1%22&occuring1=freetext&rowId=2&options2=AND&q2=&occuring2=freetext&rowId=3&options3=AND&q3=&occuring3=freetext&publishedstart=2000&publishedend=2010&calendarInput=yyyy-mm-dd&la=any&it=any&show=all&x=37&y=11 Canine adenovirus - 1 recent literature] | ||
==References== | ==References== | ||
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#Merck & Co (2008) '''The Merck Veterinary Manual (Eighth Edition)''' ''Merial'' | #Merck & Co (2008) '''The Merck Veterinary Manual (Eighth Edition)''' ''Merial'' | ||
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[[Category:Expert_Review]] | [[Category:Expert_Review]] | ||
[[Category:Respiratory_Viral_Infections]] | [[Category:Respiratory_Viral_Infections]] | ||
Revision as of 09:40, 27 September 2010
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This article has been peer reviewed but is awaiting expert review. If you would like to help with this, please see more information about expert reviewing. |
Also known as: CAV-1 - Infectious Canine Hepatitis Virus - ICH virus
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.
CAV-1 is a Mastadenovirus, member of the Adenoviridae family.
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 of the virus after shedding in the urine, faeces or respiratory secretions. Transmission may be by direct contact, or by indirect contact such as via 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.
Disease
Although there is evidence for a high incidence of infection among the non-vaccinated canine population, this is not matched by a similar occurrence 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. Bronchointerstitial pneumonia 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 parenchymal cells. Glomerulonephritis and occular pathology are not uncommon findings.
The pathology exhibited in Infectious Canine Tracheobronchitis varies with the other contributing organisms and the severity of disease.
Literature Search
Use these links to find recent scientific publications via CAB Abstracts (log in required unless accessing from a subscribing organisation).
Canine adenovirus - 1 recent literature
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
- Whittem, JH, and Blood, DC (1949) Heptatitis contagiosa canis (Rubarth) in Australia. Australian Veterinary Journal, 25
- Wright, NG, and Cornwell, HJC (1968) Viral induced neonatal disease in puppies. Journal of Small Animal Practice, 9
- Gocke, DJ et al (1970) Chronic hepatitis in the dog: the role of immune factors. J Am Vet Med Ass, 156
- Wright, NG at all (1971) Canine adenovirus nephritis. Journal of Small Animal Practice, 12
- Koptopoulos, G and Cornwell, HJC (1981) Canine adenovirusees: a review. The Veterinary Bulletin, 51(3)
- Carter, GR and Wise, DJ (2005) A Concise Review of Veterinary Virology, International Veterinary Information Service.
- Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition) Merial