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Inflammation of the brain and spinal cord.



inflammation of the brain and spinal cord as a result of infection by neurotropic viruses (acute disseminated encephalomyelitis) or as a complication of other infectious diseases, for example, measles, chicken pox, or rubella. Some cases of encephalomyelitis develop after vaccination against rabies, smallpox, and certain other diseases (postvaccinal encephalomyelitis). The inflammation may also involve the cerebrospinal roots and the peripheral nerves (encephalomyelopolyradiculoneuritis), the optic nerve or other cranial nerves (neuromyelitis optica), and the meninges (meningoencephalomyelitis).

The course of encephalomyelitis is most often acute. Symptoms include elevated body temperature, muscle pain, and various neurological symptoms (paralysis, disruption of sensitivity and motor coordination). Severe cases are marked by trophic disturbances (bedsores) and sepsis. After the acute stage, there may be residual symptoms, including paresis and disturbances of sensitivity. Treatment of encephalomyelitis is the same as for encephalitis. (See.)


Neirovirusnye infektsii. Leningrad, 1954.
Panov, A. G., and A. P. Zinchenko. Diagnostika rasseiannogo skleroza ientsefalomielita. Leningrad, 1970.




an enzootic viral disease of fur-bearing animals and swine in which the central nervous system is infected. Primarily young animals are affected. The disease occurs among fur-bearing animals in the USA and has been registered in the USSR. Teschen disease (porcine encephalomyelitis) afflicts swine in Central and Western Europe.

The causative agent of encephalomyelitis in fur-bearing animals is a neurotrophic virus; that of Teschen disease is an RNA-containing virus. Young animals are more susceptible to the disease than adults. Among fur-bearing animals, those that are afflicted include the young of foxes, including arctic foxes, and sables. Among swine, it is mainly sucklings, weaned piglets, and young being fattened that are affected.

The causative agents of the disease are introduced into the environment primarily with the saliva and nasal mucus of sick animals; in swine, it is also introduced with the feces and other excretions. Fur-bearing animals become infected through the breathing passages, while swine are infected through the respiratory and digestive tracts. The basic symptoms of the disease in fur-bearing animals include an unsteady walk, falling, convulsive attacks, the appearance of foam on the lips, and the transition from anxiety to the depressed state.

If the infection is acute, the animal dies in three to four days. Less acute cases are accompanied by a loss of appetite and diarrhea, sometimes with discharge of blood. In symptomless cases there may be abortions or the birth of nonviable young. In swine the stage of anxiety is followed by the paralysis of the extremities and of many groups of muscles. In acute cases up to 90 percent of the sick animals die; in subacute cases, up to 40 percent; and in chronic cases, up to 20 percent.

The treatment of fur bearing animals has little effect. No successful means of treating swine has been developed. In order to avoid spreading of encephalomyelitis to fur farms, animals arriving there are quarantined for one month; at swine farms the animals are inoculated with a live virus culture vaccine. When cases of the disease are discovered, and when the course of the disease is subacute, fur-bearing animals are isolated and treated with hyperimmune serum. During the winter they are slaughtered for fur. When cases of the disease are discovered in swine the entire herd is slaughtered. The meat of animals that are suspected to have the disease is processed for canning or for boiled sausage. The carcasses of sick swine or the wastes from slaughter are destroyed.

References in periodicals archive ?
Soluble recombinant complement receptor 1 inhibits inflammation and demyelination in antibody-mediated demyelinating experimental allergic encephalomyelitis.
Attenuation of experimental allergic encephalomyelitis in complement component 6-deficient rats is associated with reduced complement C9 deposition, P-selectin expression, and cellular infiltrate in spinal cords.
Abbreviations: Bad = Bcl-2-associated death promoter, Bak = Bcl-2-antagonist/killer, Bax = Bcl-2-asociated X, BBB = blood-brain barrier, Bcl-2 = B cell chronic lymphocytic leukemia/ lymphoma 2, Bid = Bcl-2 interacting domain, C5-s = C5 sufficient, C5-d = C5 deficient, CD = cluster of differentiation, CNS = central nervous system, CSF = cerebrospinal fluid, EAE = experimental allergic encephalomyelitis, Fas = cell death receptor 95/ apolipoprotein 1, IFN = interferon, IL = interleukin, MBP = myelin basic protein, MOG = myelin oligodendrocyte glycoprotein, mRNA = messenger ribonucleic acid, MS = multiple sclerosis, OLG = oligodendrocyte, PI3-K = phosphatidylinositol-3 kinase, Ser = serine, [T.
Potassium channels in T lymphocytes mediating experimental allergic encephalomyelitis (EAE) in rats.
Modulation of outward K(+) conductance is a post-activational event in rat T lymphocytes responsible for the adoptive transfer of experimental allergic encephalomyelitis.
Potassium channel blockers inhibit adoptive transfer of experimental allergic encephalomyelitis by myelin-basicprotein-stimulated rat T lymphocytes.
A good model system for MS is an animal disease found in mice, rats and guinea pigs called experimental allergic encephalomyelitis (EAE).
In mice with the MS-like disease, experimental allergic encephalomyelitis (EAE), we have known the details of the disease-specific immune response for some time and a variety of drugs including monoclonal antibodies and synthetic peptides, which block those responses in a highly specific fashion, have been extremely successful in treating this animal disease.

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