Description
Data Sheet
| Background | Canine Distemper Virus is shed in all excretions and secretions, and is spread by direct and indirect contact via ingestion or inhalation of aerosolised droplets. Initial infection of the nasal cavity, pharynx and lungs is followed by a macrophage-associated viraemia to local lymph nodes where the virus replicates. Within one week, all lymphoid tissue is infected, causing lymphopenia. A second viraemic stage then distributes the virus to the surface epithelium of the respiratory, gastrointestinal and urogenital tracts, endocrine tissue and the grey and white matter of the CNS. A biphasic pyrexia is typical of distemper infection: the first fever occurs 3-6 days post-infection and is associated with lymphopenia, and the second peak coincides with widespread viraemia. Further signs depend on both the virus strain and the immune response mounted. In the event of a strong humoral and cellular response, disease may remain subclinical, and if a weak immune response is mounted infection is generally subacute. If the immune response fails, acute disease and potentially death ensues. When clinical disease manifests, this is initially characterized by lethargy, dehydration, anorexia, and weight loss followed by more specific signs depending on the principally affected organ. Canine distemper is often fatal, but an increased production of virus-neutralizing antibodies can promote the recovery of the animal. However, CDV can persist in the uvea, CNS, lymphoid organs and footpads despite elimination from most organs and the blood. This can result in “old dog encephalitis” in dogs that recovered from acute canine distemper years previously. In this, several neurological episodes occur over weeks to months, and usually culminate in the death of the dog. |
