Difference between revisions of "Canine Adenovirus 1"

Latest revision as of 10:25, 26 May 2021

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 histologically 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.

Canine Adenovirus 1 Learning Resources
Literature Search Search for recent publications via CAB Abstract (CABI log in required)	Canine adenovirus 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

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-Causes [[Canine Infectious Tracheobronchitis]]
+{{OpenPagesTop}}
+Also known as: '''''CAV-1 — Infectious Canine Hepatitis Virus — ICH virus'''''
- CH is caused by a nonenveloped DNA virus, canine  adenovirus 1 (CAV-1), which is antigenically related only to CAV-2 (one  of the causes of infectious canine tracheobronchitis,                   Infectious Tracheobronchitis of Dogs). CAV-1 is  resistant to lipid solvents and survives outside the host for weeks or  months, but a 1-3% solution of sodium hypochlorite (household bleach) is  an effective disinfectant.
+==Introduction==
-*[[Adenoviridae|Adenoviridae]]
+Canine Adenovirus 1 (CAV-1) was first isolated by Carbasso in 1954<sup>1</sup> from a case of acute hepatitis in the dog. This virus found to be identical to the virus isolated in 1947 by Rubarth<sup>2</sup> 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 age<sup>3</sup>. It has also since been demonstrated that CAV1 has a role in diseases other than [[Infectious Canine Hepatitis]], such as [[Canine Infectious Tracheobronchitis]].
-*Usually mild [[Lungs Inflammatory - Pathology#Bronchointerstitial pneumonia|bronchointerstitial pneumonia]], necrosis of bronchiolar and alveolar epithelium, oedema, type II pneumocyte hyperplasia
-*May cause necrotising [[Bronchi and Bronchioles Inflammatory - Pathology#Infectious causes of bronchitis or bronchiolitis|bronchiolitis]] in immune-deficient dogs ([[Paramyxoviridae#Canine Distemper Virus (CDV)|distemper]])
-*Can be associated with [[Canine Infectious Tracheobronchitis|kennel cough]] described above
-====Hosts====
+CAV-1 is a Mastadenovirus, member of the [[Adenoviridae - Overview|Adenoviridae]] family.
-*Dogs
-*Foxes are very susceptible (Fox Encephalitis)
-====Epidemiology====
+==Hosts==
-*Transfers '''easily''' via ingesting infected '''urine, feces or respiratory secretions'''
+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.
-*Can be transferred by handlers, infected surfaces, etc.
+==Transmission==
-[[Image:Adenovirus pneumonia.jpg|right|thumb|100px|<small><center>Adenovirus pneumonia (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
+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.
-[[Category:Adenoviridae]][[Category:Dog]]
+==Disease==
-[[Category:To_Do_-_Lizzie]]
+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 <sup>4</sup>, ocular lesions, neonatal disease<sup>5</sup>, chronic hepatitis<sup>6</sup>, and interstitial nephritis<sup>7</sup>. 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 histologically 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.
+{{Learning
+|literature search = [http://www.cabdirect.org/search.html?rowId=1&options1=AND&q1=%22canine+adenovirus%22&occuring1=title&rowId=2&options2=AND&q2=&occuring2=title&rowId=3&options3=AND&q3=&occuring3=freetext&x=44&y=11&publishedstart=2000&publishedend=yyyy&calendarInput=yyyy-mm-dd&la=any&it=any&show=all Canine adenovirus 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''
+{{review}}
+{{OpenPages}}
+[[Category:Adenoviridae]][[Category:Dog Viruses]][[Category:Respiratory Diseases - Dog]]
+[[Category:Expert_Review]]
 [[Category:Respiratory_Viral_Infections]]