Canine distemper neuropathology

Abstract

Canine Distemper is an infectious disease of acute, subacute, and chronic clinical appearance, caused by a Morbilivirus, family Paramyxovirydae. Of worldwide distribution, no seasonal occurrence, susceptibility between males and females, or racial preference has been described. Young dogs are generally more susceptible to infection, demonstrating a relationship between susceptibility and age.

Canine Distemper virus is generally transmitted as an aerosol infection to the upper respiratory tract. After entering of the virus and invasion of epithelial tissues, viral replication into macrophages and spreading occur. Four to six days after initial infection, a new replication starts, causing a rise in body temperature and leucopenia. Eight to ten days after inoculation the virus invades various epithelial tissues and the central nervous system. Acute encephalitis, which occurs early in the course of infection in young or immunosuppressed animals, is characterized by direct viral injury. Multifocal encephalitis of chronic evolution often occurs in adult dogs between four to six years old. The old-dog encephalitis is a rare form of the disease characterized by panencephalitis that may be a persistent infection with a defective virus, usually present in animals older than six years. Characteristic demyelinating lesions are observed around three weeks post infection, during a period of massive virus-induced immunosuppression, as a consequence of viral replication inside oligodendrocites. The chronic demyelination coincides with the recovery of the immune system, characterized by reduction or lost of viral proteins, followed by upregulation of the major histocompatibility complex and inflammatory cells infiltration. The clinical course and neurological pattern of the encephalomyelitis varies depending on the virulence of the virus strain, and host age. Abnormalities like increases in protein, because elevated IgG levels, and cell count, with a predominance of lymphocytes, are detectable in cerebrospinal fluid in dogs suffering the chronic stage of the disease. It is possible to confirm infection on histologic examination by the observation of well delimited necrotic areas, demyelination and inclusion bodies. Isolation technique of virulent canine distemper virus in cell cultures is very specific and false-negative results will occur if the animal is not entere the acute phase. The reverse transcription polymerase chain reaction has shown to be useful for viral detection. A final diagnosis is based on the demonstration of viral antigens in scrapings and body fluids by immunofluorescence test. Augment in titles of IgM and IgG in serum is ambiguous because it just indicates previous and/or present infections, even in vaccinated animals. Immunosupression induced by canine distemper virus probably collaborates with varieties of opportunistic agents, i.e. Toxoplasma gondii. Live attenuated vaccines have been used successfully for many years to control wild-type morbilivirus infection.