Pathogenes Inc.

Acute Disseminated Encephalomyelitis (ADEM) can occur following a bacterial, viral, or parasitic infection.  There are similarities between EPM and post vaccinal encephalomyelitis.

Experimental autoimmune encephalomyelitis or Experimental Allergic Encephalomyelitis (EAE) is an animal model of brain inflammation. The model induces an inflammatory disease of the central nervous system (CNS),  mostly used with rodents, and is widely studied as an animal model of the human CNS diseases, including multiple sclerosis and acute disseminated encephalomyelitis (ADEM). EAE is also the model for T-cell-mediated autoimmune disease in general.

The first report of this disease was by Pasteur (1885) and was associated with an anti-rabies vaccine.  The vaccine included dried rabbit spinal tissues.  Dr.’s Rivers, Sprunt, and Berry (1933) observed that after a viral infection, in some people, an inflammatory or allergic encephalomyelitis occurred.  They reproduced the syndrome by transferring some inflamed patient tissue to primates  (Journal of Experimental Medicine article (Vol. 58, No. 1, pp. 39-56).

Experimental allergic encephalitis has been induced in a number of species, including mice, rats, guinea pigs, rabbits and primates. The various antigens (in rodents spinal cord homogenate myelin protein, dermal cells) result in distinct models with different disease characteristics regarding both immunology and pathology. Allergic encephalitis may also be induced by the passive transfer of T cells specifically reactive to the sensitizing antigens.

Depending on both the antigen used and the genetic make-up of the animal, rodents can display a single bout of EAE, a relapsing-remitting form, or chronic EAE. Clinical symptoms occur about two weeks after immunization and present with a relapsing-remitting disease. The first clinical symptom is weakness of tail tone that progresses to paralysis of the tail, followed by a progression up the body.  The disease symptoms reflect the anatomical location of the inflammatory lesions, and may also include sensory loss, optic neuritis, difficulties with coordination and balance (ataxia), and muscle weakness and spasms. Recovery from symptoms can be complete or partial and the time varies with symptoms and disease severity.

In one model of EAE researchers demonstrated that a monoclonal antibody prevented the development of experimental allergic encephalomyelitis (EAE) in mice. Furthermore, treatment with the antibody reversed EAE when the antibody was given to paralyzed animals. The mechanism of protection by injection of the antibodies was suggested as selective reduction of the number of reactive T helper cells in the spleen and the lymph nodes.  There are other treatments that have been effective in ameliorating the signs of EAE.

There are some similarities between vaccine induced reactions (post-vaccinal encephalomyelitis) in horses as well as the similarity of chronic relapsing EPM and relapsing-remitting EAE.   More information is needed to determine, if any, the relationship between these diseases that affect the CNS of horses.