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| CAV-1 infection occurs by inhalation and ingestion, after shedding in the urine, faecs or respiratory secretions. Transmission my be by direct contact, or by indirect contact and fomites such as 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. | | CAV-1 infection occurs by inhalation and ingestion, after shedding in the urine, faecs or respiratory secretions. Transmission my be by direct contact, or by indirect contact and fomites such as 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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− | ==Disease== | + | ==Clinical Features== |
− | This high incidence of infection is not matched by a similar incidence of clinical hepatitis, and it is 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).
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| + | Although there is evidence for a high incidence of infection among the non-vaccinated canine population, this is not matched by a similar occurance of clinically detectable infectious hepatitis since many infections are subclinica. The virus has also been show 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 fro some dogs with respiratory disease, and CAV-1 is of importance in [[Canine Infectious Tracheobronchitis]]. |
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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.
| + | In [[Infectious Canine Hepatitis]], clinical signs typically include depression, fever, vomiting, diarrhea, and discharges from the nose and eyes. Coagulopathies may also develop. |
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| + | ==Pathology== |
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| + | Infection with canine adenovirus 1 most typically causes a mild bronchointerstitial pneumonia, although a necrotising bronchiolitis may occur in immunocompromised dogs. This is seen histologcally as necrosis of the bronchiolar and alveolar epithelium, pulmonary oedema and hyperplasia of type II pneumocytes. |
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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 | | *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. |