| Line 27: |
Line 27: |
| | ==Pathology== | | ==Pathology== |
| | | | |
| − | 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.
| |
| | | | |
| − | *Can be associated with [[Canine Infectious Tracheobronchitis|kennel cough]] described ab
| + | Subclinical 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. |
| − | 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.
| + | In [[Canine Infectious 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 parencymal cells. Glomerulonephritis and occular pathology are not uncommon findings. |
| − | 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== | | ==References== |