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)

After an incubation period of one to two months rabies presents with non-specific prodromal symptoms and often with paraesthesiae of the bitten area. As in canine rabies there are furious and dumb forms of the disease. In man, furious rabies is characterised by hydrophobia: terror and excitation with spasms of inspiratory muscles, larynx and pharynx precipitated by attempts to drink and by a variety of other stimuli. Hydrophobia may represent an exaggerated respiratory tract irritant reflex with associated arousal potentiated by the selective destruction of brain stem inhibitory systmes. Also typical of furious rabies are intermittent episodes of excitement, hallucinations and maniacal behaviour. Focal neurological abnormalities are surprisingly uncommon. Other signs include hypersalivation, tachycardia and hyperpyrexia. Paralysis and coma supervene after a few days: survival rarely exceeds seven days. Dumb or paralytic rabies is an ascending flaccid paralysis with sphincter involvement and sensory disturbances. Death from respiratory and bulbar paralysis occurs after a longer illness than furious rabies. In a minority of cases hydrophobia develops before the terminal coma. Complications include respiratory arrest, pneumonitis, cardiac arrhythmias and interstitial myocarditis, posterior pituitary disorders, and gastrointestinal bleeding. Differential diagnoses of furious rabies include hysterical pseudo hydrophobia, tetanus, other encephalitides, delirium tremens and various other intoxications. Paralytic rabies may have to be distinguished from postvaccinal encephalomyelitis, poliomyelitis and other causes of Landry-type ascending paralysis. Intensive care has produced some promising results: life-threatening complications can be prevented but there is some evidence that the severity of the encephalitis is the ultimate barrier to survival.
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PMID:The clinical picture of rabies in man. 98 12

Serum sickness in man may occur after treatment with foreign proteins such as tetanus or diphtheria antisera, and in some patients leads to neurological complications such as neuropathy or encephalomyelitis. Many of the effects of serum sickness are associated with the deposition of antigen-antibody complexes in the tissues. Chronic serum sickness in the rabbit has previously been shown to cause perivascular inflammation and demyelination in the nervous system. We induced chronic serum sickness in the Lewis rat by daily intraperitoneal injections of bovine serum albumin (BSA) in male rats that had previously received footpad inoculations of BSA. Two animals died of anaphylaxis and 15 were observed for periods of 39 to 142 days. Three animals injected with 3 mg or 4 mg/day of BSA, and 6 animals injected with up to 16 mg/day of BSA had no clinical abnormalities when sacrificed. Six animals were injected with 36 to 40 mg BSA/day and, at the time of sacrifice, were lethargic and had ruffled fur, but no neurological signs. In these animals, the production of chronic serum sickness was confirmed by the presence of immune complex deposits in the kidneys. In the nervous system, there was no evidence of inflammatory cell infiltration either in the parenchyma or the vessel walls. Immunofluorescence studies identified deposits of immunoglobulin in the choroid plexus of chronic serum sickness rats but not in controls. Staining with antibodies to immunoglobulin, complement and BSA showed marked staining of blood vessels of the nerve roots of the animals with chronic serum sickness.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lack of neurological abnormalities in Lewis rats with experimental chronic serum sickness. 182 22

Lymphocytes were isolated from the spinal cord and draining lymph nodes of Lewis rats with acute experimental allergic encephalomyelitis (EAE) 12 days after immunization with myelin basic protein (MBP) and tetanus toxoid (TT). An average of 8.0 +/- 2.0 X 10(6) cells was obtained from the spinal cord. Of these 71.1 +/- 8.6% expressed the helper-T-cell marker W3/25 and 14.8 +/- 6.2% expressed the killer/suppressor-T-cell marker OX8. By limiting dilution analysis of cells exhibiting an antigen-specific proliferative response, the average frequencies of cells reactive to MBP and TT were 3.36 +/- 2.4 and 7.60 +/- 4.1 per 10(4), respectively. In the draining lymph nodes, the frequencies of cells reactive to MBP and TT were 2.24 +/- 1.7 and 2.69 +/- 2.5 per 10(4). At a relatively early stage of clinical EAE, MBP-reactive T cells comprise only a small minority of the cells which can be isolated from the spinal cord; lymphocytes reactive to a protein antigen irrelevant to EAE pathogenesis are present in comparable numbers. This finding suggests that most of these cells accumulate as a result of mechanisms not specific for MBP-reactive lymphocytes.
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PMID:Limiting dilution analysis of the frequency of antigen-reactive lymphocytes isolated from the central nervous system of Lewis rats with experimental allergic encephalomyelitis. 244 May 88

The pathogenesis of multiple sclerosis (MS) is thought to involve a T-cell-mediated autoimmune process. Experimental allergic encephalomyelitis (EAE), an animal model resembling MS, can be induced by immunization with myelin antigens such as myelin basic protein. The T-cell antigen receptor (TCR) usage in EAE is highly restricted in some strains of animals and experimental treatments targeting the TCR have been successful in EAE. Examination of the TCR beta-chain variable-region (V beta) usage of MBP-specific T-cell lines in MS patients has produced conflicting results. Our previous studies of TCR alpha-chain variable-region usage in monozygotic twins demonstrated a general skewing of the TCR repertoire in individuals with MS. This skewing became apparent only after stimulation with antigens; in peripheral blood lymphocyte preparations from individuals with MS V alpha 8-bearing T cells were preferentially selected by stimulation with myelin basic protein. In the present study we examined complementarity-determining region 3 of those V alpha 8-positive TCRs. Marked sequence heterogeneity was found in all individuals with severe MS. In contrast, restricted areas of complementarity-determining region 3 were found in healthy control individuals and in individuals with a mild form of MS. Sequences from tetanus toxoid-specific V alpha 8-positive T cells generated from the same individuals were relatively homogeneous within individuals regardless of disease activity and were distinct from the sequences of complementarity-determining region 3 in myelin basic protein-stimulated lines. These findings suggest that disease severity may be associated with increased heterogeneity of myelin antigen-specific T cells and could reflect an impaired ability of the immune system to down-regulate these anti-self responses.
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PMID:Heterogeneity of T-cell receptor alpha-chain complementarity-determining region 3 in myelin basic protein-specific T cells increases with severity of multiple sclerosis. 751 5

Copolymer-1 (Cop-1) inhibits the T cell response to myelin basic protein (MBP), suppresses experimental autoimmune encephalomyelitis in many animal species, and was recently shown to be effective in the treatment of multiple sclerosis (MS). Interferon beta-1b (IFN-beta), an immune modulator with no antigenic specificity, is already approved for treatment of relapsing-remitting MS. We investigated the combined effect of these two agents on the cellular immune response to MBP. Antigen-specific Th1-like cell lines were generated from two healthy individuals with different MHC phenotypes. Cop-1 inhibited the proliferation of all MBP-specific lines but had no suppressive effect on tuberculin (PPD) or tetanus toxoid (TT)-specific T cell lines from either donor, while IFN-beta non-specifically reduced proliferation of all T cell lines. When combined in vitro, Cop-1 and IFN-beta had additive suppressive effects on proliferation of MBP-specific T cell lines, with 70-100% inhibition depending on the concentration of antigen. Synthesis of the pro-inflammatory cytokines interleukin-2 and IFN-gamma by MBP-specific lines was also inhibited additively (up to 100%). When antigen-presenting cells (APC) were pretreated with Cop-1, IFN-beta or both, T cell proliferation was inhibited in the same additive pattern, even though the inhibitors were not present in culture, indicating that they acted primarily through modulation of APC function. Additive effects were not found with PPD- or TT-specific cell lines. Pretreatment of APC with IFN-beta resulted in dose-dependent reduction in HLA-DR and HLA-DQ expression, which paralleled inhibition of T cell proliferation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Additive effects of copolymer-1 and interferon beta-1b on the immune response to myelin basic protein. 759 54

To help understand effector mechanisms in experimental allergic encephalomyelitis (EAE) we examined the effects of adding 'irrelevant' lymphocytes from non-EAE donors to major basic protein (MBP)-reactive lymphocytes in the adoptive transfer of EAE (Tr-EAE). The intravenous injection of tetanus toxoid-reactive lymphocytes (TT-cells) and phytohemagglutinin-stimulated lymphocytes on the same day or 2 days after intra-arterial injection of MBP-reactive lymphocytes enhanced the clinical and pathological expression of Tr-EAE. In lymphocyte trafficking studies there was significant accumulation of these injected TT-cells in the central nervous system during enhanced transfer of EAE. W3/25-positive cells were much more predominant in lesion of central nervous system when reinjected with TT cells along with MBP cells compared with lesions of rats injected with MBP cells alone. These findings suggest possible participation of lymphocytes other than MBP-reactive cells in the expression of EAE and provide a useful model to further explore effector mechanisms in the future.
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PMID:Enhancing effects of irrelevant lymphocytes on adoptive transferred experimental allergic encephalomyelitis. 842 7

We report the assessment by MRI of a case of radiculomyelitis after vaccination against tetanus-poliomyelitis. In the acute stage the appearance was an isolated myelitis of the conus medullaris with contrast enhancement. The upper thoracic cord presented central areas of high signal intensity on T2 weighted images. Rapid clinical recovery was correlated with resolution of abnormal enhancement. Follow-up MR at 5 months showed persistence of slight T2 prolongation in the conus medullaris and syringohydromyela of the thoracic cord. A single lesion of the spinal cord is a rare presentation of acute disseminated encephalomyelitis, the course of such lesions, to date not previously displayed by MR, is unknown. Proper diagnosis should help prevent administration of further vaccine doses.
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PMID:[Postvaccination myelitis. Aspect and course followed by MRI]. 876 35

The primary lesions of eastern equine encephalomyelitis (EEE) virus infection in the horse are limited to the brain and spinal cord. Intestinal lesions in addition to the changes in the central nervous system were found in a 6-month-old male Tennessee Walking Horse. One week prior to death, this colt was vaccinated for EEE virus, western equine encephalomyelitis virus, influenza virus, equine rhinopneumonitis virus, and tetanus. The clinical signs consisted of ataxia and rear-end weakness, with a body temperature of 102.8 F. Gross lesions consisted of yellowish discoloration, swelling, edema, and hemorrhage of the brain stem and dark discoloration of the gray matter of the spinal cord. Microscopic lesions in the small intestine were mainly in the muscular layer and consisted of multifocal areas of myonecrosis and lymphomonocytic infiltration with a few focal areas of mild fibrous connective tissue proliferation. Occasional focal mild perivascular lymphocytic infiltration was observed in the submucosa. Lesions in the brain and spinal cord consisted of widespread areas of perivascular lymphomonocytic cuffing, focal areas of necrosis, neutrophilic infiltration, hemorrhage, neuronal degeneration, and gliosis. Hepatic changes consisted of periportal lymphocytic infiltration and mild vacuolar degeneration of hepatocytes. EEE virus was isolated from the intestine and detected by DNA in situ hybridization.
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PMID:Intestinal lesions in a horse associated with eastern equine encephalomyelitis virus infection. 982 95

Copolymer-1 (Copaxone or COP) inhibits experimental allergic encephalomyelitis and has beneficial effects in multiple sclerosis. There is presently no practical in vitro assay for monitoring the immunological effects of COP. We used an automated, computer-assisted enzyme-linked immunoadsorbent spot assay for detecting COP-induced interferon-gamma (IFN-gamma)- and interleukin-4 (IL-4)-producing cells and a standard proliferation assay to assess the immunological response to COP in peripheral blood mononuclear cells from 20 healthy donors, 20 untreated multiple sclerosis patients and 20 COP-treated multiple sclerosis patients. Compared with untreated and healthy controls, COP-treated patients showed (i) a significant reduction of COP-induced proliferation; (ii) a positive IL-4 Elispot response mediated predominantly by CD4 cells after stimulation with a wide range of COP concentrations; and (iii) an elevated IFN-gamma response partially mediated by CD8 cells after stimulation with high COP concentrations. All three effects were COP-specific as they were not observed with the control antigens, tuberculin-purified protein or tetanus toxoid. The COP-induced changes were consistent over time and allowed correct identification of COP-treated and untreated donors in most cases. We propose that these criteria may be helpful to monitor the immunological response to COP in future clinical trials.
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PMID:Treatment of multiple sclerosis with Copaxone (COP): Elispot assay detects COP-induced interleukin-4 and interferon-gamma response in blood cells. 1128 71

Although vaccine manufacturers make no specific recommendations regarding the vaccination of older horses and ponies, the similarities in age-induced immunologic changes between human beings and equids suggests that similar vaccination recommendations should be followed. The need for vaccination of the older horse depends, of course, on the relative risk of exposure for the individual horse. Particular care should be taken when using attenuated vaccine products because these live agents may pose a unique risk to the older individual. Immunization with inactivated agent vaccines is likely to be safer. In general, annual vaccination against equine influenza virus infection, tetanus, rabies, and encephalomyelitis viruses is warranted.
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PMID:The effect of aging on immune responses. 1251 37


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