Canine distemper virus is a paramyxovirus. The fragile, enveloped, single-strand RNA virus is sensitive to most disinfectants, including phenols and quaternary ammonium compounds. It is relatively unstable outside the host. The main route of infection is via aerosol droplet secretions from infected animals.
Some infected dogs may shed virus for several months.
The virus initially replicates in the lymphatic tissue of the respiratory tract. A cell-associated viremia results in infection of all lymphatic tissues, which is followed by infection of respiratory, GI, and urogenital epithelium, as well as the CNS and optic nerves. Disease follows virus replication in these tissues. The degree of viremia and extent of viral spread to various tissues is moderated by the level of specific humoral immunity in the host during the viremic period.
A transient fever usually occurs 3–6 days after infection, and there may be a leukopenia (especially lymphopenia) at this time; these signs may go unnoticed or be accompanied by anorexia. The fever subsides for several days before a second fever occurs, which may be accompanied by serous nasal discharge, mucopurulent ocular discharge, lethargy, and anorexia. GI and respiratory signs, typically complicated by secondary bacterial infections, may follow; rarely, pustular dermatitis may be seen. Encephalomyelitis may occur in association with these signs, follow the systemic disease, or occur in the absence of systemic manifestations. Dogs surviving the acute phase may have hyperkeratosis of the footpads and epithelium of the nasal planum, as well as enamel hypoplasia in incompletely erupted teeth.
Overall, a longer course of illness is associated with the presence of neurologic signs; however, there is no way to anticipate whether an infected dog will develop neurologic manifestations. Classic neurologic signs include: localized involuntary muscle twitching, convulsions, excessive salivation and chewing movements of the jaw, circling, head tilt, generalized seizures and paralysis.
A dog may exhibit any or all of these multisystemic signs during the course of the disease. Infection may be mild and inapparent or lead to severe disease with most of the described signs. The course of the systemic disease may be as short as 10 days, but the onset of neurologic signs may be delayed for several weeks or months as a result of chronic progressive demyelination within the CNS.
Clinicopathologic findings are nonspecific and include lymphopenia, with the possible finding of viral inclusion bodies in circulating leukocytes very early in the course of the disease. Thoracic radiographs may reveal an interstitial pattern typical of viral pneumonia.
Thymic atrophy is a consistent postmortem finding in infected young puppies. Hyperkeratosis of the nose and footpads is often found in dogs with neurologic manifestations. Depending on the degree of secondary bacterial infection, bronchopneumonia, enteritis, and skin pustules also may be present. In cases of acute to peracute death, exclusively respiratory abnormalities may be found. Histologically, canine distemper virus produces necrosis of lymphatic tissues, interstitial pneumonia, and cytoplasmic and intranuclear inclusion bodies in respiratory, urinary, and GI epithelium.
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