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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+{{OpenPagesTop}}
+Also known as: '''''CAV-1 — Infectious Canine Hepatitis Virus — ICH virus'''''
 ==Introduction==
 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]].
-==Classification==
+CAV-1 is a Mastadenovirus, member of the [[Adenoviridae - Overview|Adenoviridae]] family.
-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.
+==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.
-==Viral Characteristics==
+==Transmission==
-[[Image:Adenovirus.jpg|thumb|150px|Right]]
-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.
+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.
-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.
+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.
-==Hosts==
+==Disease==
-*Dogs
-*Foxes are very susceptible (Fox Encephalitis)
-Occurrence
+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]].
-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.
+==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.
-==Transmission and Epidemiology==
+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.
-*Transfers '''easily''' via ingesting infected '''urine, feces or respiratory secretions'''
+The pathology exhibited in [[Infectious Canine Tracheobronchitis]] varies with the other contributing organisms and the severity of disease.
-*Can be transferred by handlers, infected surfaces, etc
-Infection is by inhalation and ingestion. Spread is by direct and indirect contact.
+{{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]
+}}
-The virus replicates initially in tonsils and Peyer’s  patches  producing a viremia with secondary localization and replication  in the  liver and kidney
+==References==
-.
-==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).
+#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''
-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.
+{{review}}
-*[[Adenoviridae|Adenoviridae]]
+{{OpenPages}}
-*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 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)'''
-[[Image:Adenovirus pneumonia.jpg|right|thumb|100px|<small><center>Adenovirus pneumonia (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
+[[Category:Adenoviridae]][[Category:Dog Viruses]][[Category:Respiratory Diseases - Dog]]
-[[Category:Adenoviridae]][[Category:Dog]]
+[[Category:Expert_Review]]
-[[Category:To_Do_-_Lizzie]]
 [[Category:Respiratory_Viral_Infections]]