Difference between revisions of "Canine Adenovirus 1"

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==Introduction==
 
==Introduction==
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Causes [[Canine Infectious Tracheobronchitis]]
  
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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.
 
==Classification==
 
==Classification==
  
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They are resistant to trypsin and lipid solvents, and moderately resistant on premises.
 
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
 
Figure  13-1. Adenoviridae (70 - 90 nm). Note the fiber proteins protruding  from the vertices of the 12 pentons. To view click on figure
==Transmission and Epidemiology==
 
==Disease==
 
his family consists of double-stranded DNA viruses with an  icosahedral nucleocapsid. They have been recovered from many mammalian  and avian species. Many are found in the respiratory tract and  infections are often persistent. Only a small number cause significant  veterinary diseases. 
 
Viral Characteristics
 
  
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==Hosts==
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*Dogs
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*Foxes are very susceptible (Fox Encephalitis)
  
 
Occurrence
 
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.
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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.
Transmission
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==Transmission and Epidemiology==
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*Transfers '''easily''' via ingesting infected '''urine, feces or respiratory secretions'''
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*Can be transferred by handlers, infected surfaces, etc
 
Infection is by inhalation and ingestion. Spread is by direct and indirect contact.
 
Infection is by inhalation and ingestion. Spread is by direct and indirect contact.
Pathogenesis
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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.
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Clinical & Pathologic Features
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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
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.
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==Disease==
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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.
 
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.
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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]])
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*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.
 
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.
 
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.
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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.
 
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.
 
These core canine vaccines were traditionally administered annually but are now, depending on the type of vaccine, often given less frequently.
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Causes [[Canine Infectious Tracheobronchitis]]
 
 
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.
 
*[[Adenoviridae|Adenoviridae]]
 
*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====
 
*Dogs
 
*Foxes are very susceptible (Fox Encephalitis)
 
 
====Epidemiology====
 
*Transfers '''easily''' via ingesting infected '''urine, feces or respiratory secretions'''
 
*Can be transferred by handlers, infected surfaces, etc.
 
 
  
 
[[Image:Adenovirus pneumonia.jpg|right|thumb|100px|<small><center>Adenovirus pneumonia (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
 
[[Image:Adenovirus pneumonia.jpg|right|thumb|100px|<small><center>Adenovirus pneumonia (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]

Revision as of 11:52, 6 August 2010

Introduction

Causes Canine Infectious Tracheobronchitis

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. 

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

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.

Adenovirus pneumonia (Image sourced from Bristol Biomed Image Archive with permission)