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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The DA virus is a neurotropic murine virus which can induce acute encephalomyelitis in suckling mice and a chronic myelopathy in weanlings. The agent has been attenuated by serial passage in baby hamster kidney (BHK-21) cells. When attenuated virus is inoculated in 8-week-old C3HeJ mice a myelopathy of delayed onset with prominent demyelination of lateral and anterior columns occurs. The DA virus is believed to be related to the Theiler murine encephalomyelitis (TME) viruses because of the similar clinical and pathological conditions which it causes, and because neutralization tests indicate shared antigens between it and GD7, a TME virus. This paper reports electron-microscopic studies of BHK-21 cells infected with DA virus. The cells were prepared 24 and 48 hr after inoculation. Cytopathic effects were observed and infected cells contained plaques consisting of numerous 25 nm virus particles in crystalline array. The virions were exclusively intracytoplasmic and were morphologically indistinguishable from human poliomyelitis virus. These observations appear to establish DA as a picorna virus, related to the TME virus group. The chronic myelopathy caused by DA may prove relevant to chronic demyelinative myelopathies in man, such as multiple sclerosis, and also to amyotrophic lateral sclerosis.
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PMID:Electron-microscopic appearance of the DA virus, a demyelinating murine virus. 19 12

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

RNA transcripts derived from recombinant chimeras between the highly virulent GDVII virus and the less virulent BeAn virus were constructed to study the molecular pathogenesis of Theiler's murine encephalomyelitis virus infection. The presence of the BeAn 5' noncoding sequences in chimera 2 (BeAn 5' noncoding sequences joined with the GDVII nucleotides encoding the polyprotein and present in the 3' end) resulted in dramatic attenuation of GDVII neurovirulence and development of poliomyelitis in mice. This reduced neurovirulence was associated with slower virus growth and lower peak titers in the brain and spinal cord than with parental GDVII virus replication. On the other hand, the sites of replication following chimera 2 infection were the same as those seen in GDVII-infected mice; the distribution of virus antigen and histopathological changes indicated that chimera 2 replicates in neurons in the brain, e.g., in the neocortex, hippocampus, caudate putamen, and brain stem, as well as in anterior-horn cells in the spinal cord. Chimera 2 was efficiently cleared from the mouse central nervous system by day 30 postinfection, in marked contrast to the persistence of the BeAn parent in the central nervous system. This suggests that elements in the BeAn sequences that encode the polyprotein or are present in the 3' noncoding region are necessary for viral persistence. It is of interest that chimera 2-infected mice developed localized inflammatory, demyelinating lesions which were detected at day 28 postinfection but these lesions did not become larger with time. Thus, virus persistence appears to be required for maintenance and progression of immune-mediated demyelination. If the demyelinating lesions become sufficiently large, clinical signs and disease may develop.
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PMID:The 5' noncoding sequences from a less virulent Theiler's virus dramatically attenuate GDVII neurovirulence. 207 55

Infection of athymic (nu/nu) mice with Theiler's murine encephalomyelitis virus results in an acute encephalitis which resembles poliomyelitis. Immunohistochemistry and in situ hybridization were used to delineate the presence of viral proteins and RNA in the nervous systems of nude mice infected with the Daniels strain of Theiler's virus. This system permits the analysis of a viral infection in the absence of an effective immune response. By immunohistochemistry, viral antigen was found in the processes and cell bodies of neurons and glial cells. Besides the presence of viral antigen in these cell types, by in situ hybridization, Theiler's virus RNA was also found in cells associated with vascular endothelium in the brains and spinal cords of these infected mice. Theiler's virus RNA-positive endothelial cells were observed not only near the primary lesions but also away from demonstrable lesions in normal-appearing regions in the central nervous system. Earlier work had suggested an intra-axonal dissemination for this virus (M. C. Dal Canto and H. L. Lipton, Am. J. Pathol. 106:20-29, 1982). Our findings are consistent with this model but also suggest an additional mechanism for virus spread within the central nervous system, i.e., by infecting vascular cells and crossing the blood-brain barrier. Lastly, after Theiler's murine encephalomyelitis virus infection, not only glial cells but also endothelial cells express major histocompatibility complex class II (la) antigen on their surface (M. Rodriguez, M. L. Pierce, and E. A. Howie, J. Immunol. 138:3438-3442, 1987). Our demonstration of Theiler's virus-infected endotheliumlike cells may explain interactions of virus products in stimulating antigen presentation.
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PMID:Theiler's virus infection in nude mice: viral RNA in vascular endothelial cells. 284 61

Theiler's murine encephalomyelitis virus (TMEV) gives rise to a biphasic disease of the central nervous system (CNS) following intracranial inoculation of susceptible strains of mice. The early phase, during the first month, resembles poliomyelitis and in the late phase the mice suffer from inflammatory demyelination reminiscent of multiple sclerosis. In order to investigate the role of helper T cells in the acute and chronic phases of the disease we depleted mice of their L3T4 T cells in vivo with rat monoclonal antibodies, prior to infection and prior to the onset of clinical signs of demyelination. Mice depleted of their helper cells failed to produce antibodies to TMEV and consequently were unable to clear virus from the CNS and died within the first month of infection. Depletion of T cells before the demyelinating phase of the disease resulted in a marked decrease in the incidence of disease from 77% of the immunocompetent animals with clinical signs of paralysis to 36%. Immunocompetent TMEV-infected mice also developed antibodies against myelin suggesting that autoimmune mechanisms may play a role in TMEV-induced demyelination.
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PMID:The effect of L3T4 T cell depletion on the pathogenesis of Theiler's murine encephalomyelitis virus infection in CBA mice. 295 60

Comparative investigations of Sendai virus, pneumonia virus of mice (PVM), mouse encephalomyelitis virus (mouse polio), minute virus of mice (MVM), and reovirus type 3 (Reo 3) infected murine colonies revealed a 30% higher incidence of positive sera when enzyme-linked immunosorbent assay (ELISA) was employed instead of hemagglutination inhibition (HI) tests. Equivalent sensitivity as in the ELISA was obtained when the same sera were investigated by indirect immunofluorescence (IF) tests. The virus purification techniques described resulted in highly suitable antigens for all indirect ELISA established. Since IIF requires no purified antigens, this test is recommended as an alternative to ELISA as well as to HI and complement fixation (CF) tests for laboratories lacking the necessary equipment for high speed centrifugation. A high incidence of false positive HI reactions was found particularly in Reo 3 routine serology. An updated survey of seromonitoring showed that European murine colonies appeared to be infected far less with Reo 3 if ELISA or IIF tests were employed. During 1982-1984, only 13% of the mouse colonies screened possessed Reo 3 positive sera whereas no natural Reo 3 infection was found in rat colonies. Mouse hepatitis virus (MHV) and the coronaviruses of rats exhibited the highest incidence in murine colonies. A total of 60% of mouse and 41% of rat colonies were found to be infected by these viruses. In comparison with earlier serological surveys, the relative incidence of other murine infections was similar. Antibodies against Bacillus piliformis (Tyzzer's disease) were detected by the IIF test in 41% of the rat colonies screened.
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PMID:Diagnosis of murine infections in relation to test methods employed. 301 10

Weanling mice develop an acute encephalomyelitis with high mortality after intracerebral inoculation of neuroadapted Sindbis virus. The mice develop kyphoscoliosis and hindlimb paralysis. Immunohistochemical and in situ hybridization studies have demonstrated virus in the gray matter of the brain and spinal cord. Ventral horn cells are prominently infected, providing an anatomical basis for the clinical poliomyelitis. A novel route of spread of inoculated virus within the central nervous system has been found. The virus enters the ventricular system, and then travels caudally in the central canal of the spinal cord where ependymal cells are infected. The virus subsequently spreads into the gray matter. The distribution of virus in the spinal cord is likely dependent both on variations in the susceptibility of neural cells and on this route of entry and subsequent spread.
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PMID:The pathogenesis of spinal cord involvement in the encephalomyelitis of mice caused by neuroadapted Sindbis virus infection. 303 69

The repeated isolation of fixed rabies virus from the CNS tissues of victims of an acute and lethal outbreak of encephalomyelitis in Fortaleza, Brazil, in November 1960, following vaccination with a locally produced killed-virus anti-rabies vaccine of the Fermi type is considered as definitive evidence of the rabic etiology (vaccinal fixed-virus rabies, rage de laboratoire) of this outbreak. Eighteen persons were affected, all of whom died.The clinical picture of paralytic rabies was recognizable in all of these 18 patients. The well-marked characteristics of an acute infection permit the easy differentiation of the paralysis caused by fixed rabies virus from post-vaccinal accidents that occur as allergic reactions.The incriminated anti-rabies vaccine was found to contain fixed live rabies virus at a titre of 10(-3.0). After one year of storage under refrigeration, the vaccine still contained fixed rabies virus, at a titre of 0,2x10(-1.0).Subsequent laboratory studies tend to indicate that the curve of inactivation of fixed virus by phenol does not follow a linear function but rather resembles the curve of inactivation of poliomyelitis virus by heat and formol according to the Salk technique. It is suggested that the antigenicity of the so-called "killed-virus" anti-rabies vaccines is actually due to the presence in them of residual amounts of live virus.
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PMID:An outbreak of post-vaccinal rabies (rage de laboratoire) in Fortaleza, Brazil, in 1960. Residual fixed virus as the etiological agent. 529 89

The clinical and pathologic manifestation of Theiler's murine encephalomyelitis are age related. Animals infected during the first week of life die of a fulminant encephalitis analogous to human poliomyelitis. By contrast, animals infected within 2 and 4 weeks of age survive but develop chronic relapsing demyelination and persistent infection of the central nervous system. The neonatal infection results in widespread necrosis beginning with neuronal vacuolar degeneration followed by inflammatory infiltrates. Electron microscopy reveals paracrystalline arrays of 27-nm viral particles characteristic of picornaviruses within neurons and macrophages. In addition, oligodendrocytes show reactive changes and intracytoplasmic vacuoles. Immunoperoxidase studies show viral antigen primarily localized within neurons of the cerebral cortex, basal ganglia, hippocampus, and anterior horn cells. Viral antigen is found within the apical dendrites and axonal projections of hippocampal pyramidal cells suggesting that Theiler's murine encephalomyelitis may travel intraaxonally.
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PMID:Neonatal infection with the Daniels strain of Theiler's murine encephalomyelitis virus. 636 74

The histopathologic and virologic features of several mouse strains inoculated with the C strain of lactate dehydrogenase-elevating virus are described. Young C58 and AKR mice were found to develop histologic poliomyelitis when injected with cyclophosphamide prior to peripheral inoculation of lactate dehydrogenase-elevating virus. None of the C58 mice developed serious hindlimb paralysis, but some of the AKR mice did. Chronic poliomyelitis persisted for many weeks after infection in some C58 mice, but a spongioform poliomyopathy of the anterior horn was found in others. In contrast, inoculation of young C57BR/cd mice with lactate dehydrogenase-elevating virus produced inflammatory lesions restricted to central nervous system white matter that could be detected many weeks after infection. The most frequent findings were moderate leptomeningitis and myelitis localized to the white matter, however, radiculitis was also occasionally observed. Severe necrosis of spinal cord white matter was seen rarely. Development of lesions in C57BR/cd mice did not require immunosuppression prior to peripheral inoculation with virus and was not age related, sex linked, or exclusively controlled by the H-2 histocompatibility locus. Lactate dehydrogenase-elevating virus-infected C57L, C57BL/6, and RF mice did not develop poliomyelitis; however, C57L and C57BL/6 mice displayed a low incidence of mild encephalomyelitis. Poliomyelitis-susceptible C58 mice had the highest levels of viral infectivity in plasma and central nervous system tissues. White matter disease-susceptible C57BR/cd mice had viral titers in plasma and central nervous system tissues comparable to poliomyelitis-resistant C57L, C57BL/6, and RF mice. These studies demonstrate that different strains of mice have differing susceptibilities to the development of central nervous system inflammatory diseases.
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PMID:Mouse strain-specific central nervous system lesions associated with lactate dehydrogenase-elevating virus infection. 688 86


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