Difference between revisions of "Canine Adenovirus 1"

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==Introduction==
Also known as: '''''CAV-1 — Infectious Canine Hepatitis Virus — ICH virus'''''
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==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]].
 
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]].
  
CAV-1 is a Mastadenovirus, member of the [[Adenoviridae - Overview|Adenoviridae]] family.
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==Classification==
  
==Hosts==
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Canine adenovirus 1 (CAV1) is a member of the Adenoviridae family. The  Adenoviridae are a family of double-stranded DNA viruses which have an  icosahedral nucleocapsid and have been isolated from many mammals and  birds. However, only a small number of Adenoviridae cause significant  veterinary disease, one of these being canine adenovirus 1.
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.
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Classification
 +
This family originally  consisted of only two genera, Mastadenovirus, which infect mammals, and  Aviadenovirus, which infect birds. There are also several as yet  unassigned and recently assigned viruses in the family.
 +
Mastadenovirus
 +
This  genus consists of 20 virus species that infect mammals including  canine, equine, bovine, ovine and porcine adenoviruses. All 20 species  share a common antigen. Important diseases are infectious canine  hepatitis, canine adenovirus 2 infection, and equine adenovirus A  infection.
 +
Aviadenovirus
 +
This genus  includes the viruses of inclusion body hepatitis, quail  bronchitis, marble spleen disease and a number of adenoviruses of  poultry and birds  that are not associated with significant diseases.  Members of the genus share a common antigen.
 +
Previously Unassigned Adenoviruses
 +
Included  in this category are the viruses that have recently (2002) been placed  in the genera Atadenovirus and Siadenovirus. These viruses include the egg drop syndrome virus (Atadenovirus), turkey hemorrhagic enteritis  (Siadenovirus), adenoviral splenomegaly of chickens (Atadenovirus) and ovine adenovirus 287 (Atadenovirus; of research interest, but of no  disease significance) and some bovine adenovirus types 4 to 8  (Atadenovirus).
 +
MastadenovirusInfectious Canine HepatitisCause
 +
Canine adenovirus 1. The DNA sequence of this virus has been determined.
 +
==Viral Characteristics==
 +
Non-enveloped, viruses with icosahedral symmetry containing a single, linear molecule of double-stranded DNA.
  
==Transmission==
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The  capsid consists of capsomeres (called hexons) and 12 vertex capsomeres  (called pentons). These are the only viruses with a fiber (the fiber  antigen) protruding from each of the 12 pentons (see Fig. 13-1).
 +
The fiber is the structure of attachment to host cells and is also a type specific hemagglutinin.
 +
The hexon of mammalian adenoviruses contains a cross-reacting group antigen.
 +
The fiber antigen attaches to a specific cell receptor and initiates replication.
 +
The  dsDNA encodes approximately 30 proteins. Viral DNA replication,  mRNA  transcription and virion assembly occur in the nucleus, utilizing  both  host and virus-encoded factors. This results in the formation of  basophilic and / or acidophilic intranuclear inclusions.
 +
Many  adenoviruses agglutinate red cells of various animal species  and some  are capable of malignant transformation in tissue culture cell  and  oncogenesis when inoculated into laboratory animals.
 +
They are resistant to trypsin and lipid solvents, and moderately resistant on premises.
 +
Figure  13-1. Adenoviridae (70 - 90 nm). Note the fiber proteins protruding  from the vertices of the 12 pentons. To view click on figure
  
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.
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==Hosts==
 +
*Dogs
 +
*Foxes are very susceptible (Fox Encephalitis)
  
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.
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Occurrence
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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.
  
==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 <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]].
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==Transmission and Epidemiology==
  
==Pathology==
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*Transfers '''easily''' via ingesting infected '''urine, feces or respiratory secretions'''
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.  
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*Can be transferred by handlers, infected surfaces, etc
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Infection is by inhalation and ingestion. Spread is by direct and indirect contact.
  
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.
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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).
  
{{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==
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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.
  
#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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*[[Adenoviridae|Adenoviridae]]
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*Usually  mild [[Lungs Inflammatory - Pathology#Bronchointerstitial  pneumonia|bronchointerstitial pneumonia]], necrosis of bronchiolar and  alveolar epithelium, oedema, type II pneumocyte hyperplasia
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*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.
  
{{review}}
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==References==
 
 
{{OpenPages}}
 
  
[[Category:Adenoviridae]][[Category:Dog Viruses]][[Category:Respiratory Diseases - Dog]]
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*Koptopoulos, G and Cornwell, HJC (1981) Canine adenovirusees: a review. ''The Veterinary Bulletin'', '''51(3)'''
 +
*Rubarth, S (1947) An acute virus disease with liver lesions in dogs (heptatitis contagiosa canis). ''Acta Path Microbiol Scand'', '''Supplement 67'''
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*Carbasso, VJ et al (1954) Propagation of infectious canine hepatitis virus in tissue culture. ''Proc Soc Exp Biol Med'', '''85'''
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[[Image:Adenovirus pneumonia.jpg|right|thumb|100px|<small><center>Adenovirus pneumonia (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
  
  
[[Category:Expert_Review]]
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[[Category:Adenoviridae]][[Category:Dog]]
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[[Category:To_Do_-_Lizzie]]
 
[[Category:Respiratory_Viral_Infections]]
 
[[Category:Respiratory_Viral_Infections]]

Revision as of 12:23, 6 August 2010

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

Canine adenovirus 1 (CAV1) is a member of the Adenoviridae family. The Adenoviridae are a family of double-stranded DNA viruses which have an icosahedral nucleocapsid and have been isolated from many mammals and birds. However, only a small number of Adenoviridae cause significant veterinary disease, one of these being canine adenovirus 1. Classification This family originally consisted of only two genera, Mastadenovirus, which infect mammals, and Aviadenovirus, which infect birds. There are also several as yet unassigned and recently assigned viruses in the family. Mastadenovirus This genus consists of 20 virus species that infect mammals including canine, equine, bovine, ovine and porcine adenoviruses. All 20 species share a common antigen. Important diseases are infectious canine hepatitis, canine adenovirus 2 infection, and equine adenovirus A infection. Aviadenovirus This genus includes the viruses of inclusion body hepatitis, quail bronchitis, marble spleen disease and a number of adenoviruses of poultry and birds that are not associated with significant diseases. Members of the genus share a common antigen. Previously Unassigned Adenoviruses Included in this category are the viruses that have recently (2002) been placed in the genera Atadenovirus and Siadenovirus. These viruses include the egg drop syndrome virus (Atadenovirus), turkey hemorrhagic enteritis (Siadenovirus), adenoviral splenomegaly of chickens (Atadenovirus) and ovine adenovirus 287 (Atadenovirus; of research interest, but of no disease significance) and some bovine adenovirus types 4 to 8 (Atadenovirus). MastadenovirusInfectious Canine HepatitisCause Canine adenovirus 1. The DNA sequence of this virus has been determined.

Viral Characteristics

Non-enveloped, viruses with icosahedral symmetry containing a single, linear molecule of double-stranded DNA.

The capsid consists of capsomeres (called hexons) and 12 vertex capsomeres (called pentons). These are the only viruses with a fiber (the fiber antigen) protruding from each of the 12 pentons (see Fig. 13-1). The fiber is the structure of attachment to host cells and is also a type specific hemagglutinin. The hexon of mammalian adenoviruses contains a cross-reacting group antigen. The fiber antigen attaches to a specific cell receptor and initiates replication. The dsDNA encodes approximately 30 proteins. Viral DNA replication, mRNA transcription and virion assembly occur in the nucleus, utilizing both host and virus-encoded factors. This results in the formation of basophilic and / or acidophilic intranuclear inclusions. Many adenoviruses agglutinate red cells of various animal species and some are capable of malignant transformation in tissue culture cell and oncogenesis when inoculated into laboratory animals. They are resistant to trypsin and lipid solvents, and moderately resistant on premises. Figure 13-1. Adenoviridae (70 - 90 nm). Note the fiber proteins protruding from the vertices of the 12 pentons. To view click on figure

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.


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

  • Koptopoulos, G and Cornwell, HJC (1981) Canine adenovirusees: a review. The Veterinary Bulletin, 51(3)
  • 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
Adenovirus pneumonia (Image sourced from Bristol Biomed Image Archive with permission)