Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four litters of German Shorthaired Pointers from one owner developed a toxoplasmosis-like illness. According to the records, 29 of 39 dogs had hind limb paralysis. Six dogs from 2 litters were necropsied and had generalized encephalomyelitis. Tachyzoites and tissue cysts of Neospora caninum were found in the brain and spinal cord of each dog. Lesions were found in the eyes, extraocular muscles, or both in all of the dogs, and N caninum was detected microscopically in the eyes (retina and choroid in 1 dog), extraocular muscles, or both in 5 of the 6 dogs. Ocular lesions consisted of focal retinitis, choroiditis, mild nonspecific iridocyclitis, and myositis of extraocular muscles. Organisms stained with anti-N caninum serum, but not with anti-Toxoplasma gondii serum in an immunohistochemical test, except in 1 dog. In one dog, aged thick-walled N caninum tissue cysts reacted mildly with anti-T gondii serum.
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PMID:Repeated transplacental transmission of Neospora caninum in dogs. 222 66

Powassan virus strain M794, a member of the Flavivirus genus known to infect man and animals in Canada, was inoculated intracerebrally into rabbits and horses. No clinical signs were observed in rabbits, but widespread encephalitis resulted, characterized by lymphoid perivascular cuffing, lymphocytic meningitis, and lymphocytic choroiditis. In horses, eight days after inoculation, prominent neurological signs occurred and lesions were those of non-suppurative encephalomyelitis, neuronal necrosis, and focal parenchymal necrosis. The virus could not be reisolated from the rabbit or horse brains. Pathologic features, useful in separating some of the common North American equine neurological diseases, are discussed.
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PMID:Powassan viral encephalitis: a review and experimental studies in the horse and rabbit. 299 3

A total of 12 reindeer calves (Rangifer tarandus tarandus) were given 200-1,000 infective larvae of Elaphostrongylus rangiferi and autopsied 2 1/2-196 days post inoculation (p.i.). The larvae penetrated venules of the abomasal wall and followed the bloodstream via the liver to the lungs. In the lungs the larvae entered pulmonary venules and spread to all tissues via the general circulation. Many larvae that lodged in arterial vessels outside the spinal cord migrated into the cord along the spinal nerves. Nematodes matured in the central nervous system (CNS), and then migrated to the skeletal muscles (SM) via the spinal nerve roots. Eggs were deposited into veins and carried via the venous blood to the lungs. Here, the first stage larvae hatched and entered the airways. Pathological lesions consisting of focal necroses and interstitial accumulations of inflammatory cells were observed in the abomasal wall, liver, lungs, myocardium and kidneys. Infarcts were observed in the myocardium, kidneys and CNS. Other lesions in the nervous system were encephalomyelitis, focal traumatic encephalomyelomalacia, axon and myelin sheath degenerations, meningitis, choroiditis, perineuritis, neuritis and ganglioradiculitis. A multifocal verminous pneumonia persisted from day 103 p.i., and nematode-induced inflammatory oedema was observed in the intermuscular connective tissue of the SM at 196 days p.i.
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PMID:Experimental studies of Elaphostrongylus rangiferi in reindeer (Rangifer tarandus tarandus): life cycle, pathogenesis, and pathology. 783 58

Interferon-gamma (IFN-gamma) is a pleiotropic cytokine that has been implicated in immunopathogenic mechanisms of a number of inflammatory diseases of autoimmune or infectious disease etiology. However, its exact role is still a matter of debate. In experimental mouse models, IFN-gamma has been shown to exacerbate autoimmune thyroiditis, insulin-dependent diabetes mellitus, and autoimmune neuritis while it confers protection against experimental allergic encephalomyelitis and experimental uveitis. In this study, we generated transgenic rats with constitutive expression of IFN-gamma in the eye to study its paracrine effects and to investigate whether local production of IFN-gamma also confers protection against uveitis in the rat species. We show here that chronic exposure of ocular cells to IFN-gamma results in apoptotic death of retinal ganglion cells, development of chronic choroiditis, formation of retinal in-foldings, and activation of proinflammatory genes. In contrast to its protective systemic effect in the mouse, constitutive secretion of IFN-gamma in the rat eye was found to predispose the development of severe anterior uveitis and induction of retinal degenerative processes that impair visual acuity. Our data underscore the danger in extrapolation of cytokine effects in the mouse to humans without corroborating evidence in other species.
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PMID:Expression of interferon-gamma in the lens exacerbates anterior uveitis and induces retinal degenerative changes in transgenic Lewis rats. 1022 12

The pathogenesis and migratory life cycle of Elaphostrongylus cervi were studied in four sheep and six goats killed and examined 6 days to 5 months after inoculation with infective third-stage larvae (L3). Detailed histological studies demonstrated that the L3 followed a porto-hepatic, and probably also a secondary lymphatic, migratory route from the abomasum and small intestine to the lungs, with subsequent spread via the general circulation to the central nervous system (CNS) and other tissues. In addition, the results suggested that haematogenously spread L3, arrested in arterial vessels outside the spinal cord, migrated into the cord along the spinal nerves. During migration, the L3 caused focal inflammation and necrosis in the organs and along the spinal nerve roots, and infarcts occurred in the myocardium, kidneys and CNS. Nematode development took place in the CNS. During development, there was a gradual die-off of nematodes and patent infections were not observed. However, in one animal many mature nematodes were demonstrated in the CNS. In the nervous system, the nematodes caused encephalomyelitis, focal traumatic encephalomalacia, gliosis, meningitis, choroiditis, radiculitis and perineuritis. Two goats and one sheep displayed long-lasting paraparesis starting 6 weeks after inoculation. The signs apparently resulted from nematode-induced spinal nerve root lesions. From 19 weeks after inoculation the sheep also showed signs of severe brain disturbances due to traumatic and inflammatory lesions caused by adult E. cervi in the cerebral parenchyma. We conclude that E. cervi represents a potential cause of neurological disease in small ruminants grazing areas inhabited by red deer. This is the first report confirming the infectivity of E. cervi for domestic ruminants.
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PMID:Experimental Elaphostrongylus cervi infection in sheep and goats. 1104 94

Corticosteroids are effective therapy for autoimmune diseases but serious adverse effects preclude their prolonged use. However, immune-suppressive biologics that inhibit lymphoid proliferation are now in use as corticosteroid sparing-agents but with variable success; thus, the need to develop alternative immune-suppressive approaches including cell-based therapies. Efficacy of ex-vivo-generated IL-35-producing regulatory B-cells (i35-Bregs) in suppressing/ameliorating encephalomyelitis or uveitis in mouse models of multiple sclerosis or uveitis, respectively, is therefore a promising therapeutic approach for CNS autoimmune diseases. However, i35-Breg therapy in human uveitis would require producing autologous Bregs from each patient to avoid immune-rejection. Because exosomes exhibit minimal toxicity and immunogenicity, we investigated whether i35-Bregs release exosomes that can be exploited therapeutically. Here, we demonstrate that i35-Bregs release exosomes that contain IL-35 (i35-Exosomes). In this proof-of-concept study, we induced experimental autoimmune uveitis (EAU), monitored EAU progression by fundoscopy, histology, optical coherence tomography and electroretinography, and investigated whether i35-Exosomes treatment would suppress uveitis. Mice treated with i35-Exosomes developed mild EAU with low EAU scores and disease protection correlated with expansion of IL-10 and IL-35 secreting Treg cells with concomitant suppression of Th17 responses. In contrast, significant increase of Th17 cells in vitreous and retina of control mouse eyes was accompanied by severe choroiditis, massive retinal-folds, and photoreceptor cell damage. These hallmark features of severe uveitis were absent in exosome-treated mice and visual impairment detected by ERG was modest compared to control mice. Absence of toxicity or alloreactivity associated with exosomes thus makes i35-Exosomes attractive therapeutic option for delivering IL-35 into CNS tissues.
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PMID:Interleukin 35-Producing Exosomes Suppress Neuroinflammation and Autoimmune Uveitis. 3254 55