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)

Sera from indicator chicken flocks situated in southern Alberta near Lethbridge were tested by the hemagglutination-inhibition (HI) technique for antibodies to Western, Eastern and St. Louis Encephalitis viruses during the summer and early fall of the four years 1964 to 1967.One chicken in 1964, 90 in 1965 and five each in 1966 and 1967 were positive to Western encephalomyelitis (WE) virus by hemagglutination-inhibition tests. All of the positive sera were confirmed by neutralization test (NT) in infant mice. No antibodies to the Eastern and St. Louis viruses were detected. Infection with WE virus was detected in each of the four years, indicating that WE virus is endemic to southern Alberta with a marked seasonal incidence occurring between the second week in August and the third week in September. An improved technique for filtering sera is described.
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PMID:Western encephalomyelitis virus infection in "indicator" chickens in southern Alberta. 424 74

Viruses have been found to induce inflammatory demyelinating lesions in central nervous system (CNS) tissue of both animal and man, either by natural infections or after vaccination. At least two different pathogenic mechanisms have been proposed for these changes, a cytopathic viral infection of oligodendroglia cells with subsequent cell death, and a host immune reaction against virus and brain antigens. We now report the occurrence of cell-mediated immune reactions against basic myelin proteins in the course of coronavirus infections in Lewis rats. Infection of rats with the murine coronavirus JHM leads to demyelinating encephalomyelitis developing several weeks to months postinfection. Lymphocytes from these diseased Lewis rats can be restimulated with basic myelin protein (BMP) and adoptive transfer of these cells leads to lesions resembling those of experimental allergic encephalomyelitis (EAE) in recipients, which can be accompanied by a mild clinical disease. This model demonstrates that a virus infection in CNS tissue is capable of initiating an autoimmune response which may be of pathogenic importance.
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PMID:Adoptive transfer of EAE-like lesions from rats with coronavirus-induced demyelinating encephalomyelitis. 631 Apr 11

Infection of 21-25-day-old rats with the murine coronavirus JHM was followed either by an acute encephalomyelitis (AE) or subacute demyelinating encephalomyelitis (SDE). The major neuropathological finding in AE, which developed within 6-12 days p.i. consisted of necrotizing lesions distributed mainly in the grey matter of the central nervous system (CNS). SDE developed 14-30 days p.i. and affected rats revealed lesions of primary demyelination with predilection sites in the white matter. The time-course for the development of lesions, virus replication and neutralizing antiviral antibody production within the first 3 weeks p.i. were studied. Within the first 2 weeks p.i., most rats showed no clinical signs but nevertheless revealed lesions typical of AE. In parallel to these neuropathological changes infectious virus could be isolated from brain and spinal cord. However, coinciding with multiplication of neutralizing JHM antibodies 10-12 days after infection no infectious virus was recoverable from CNS material. At this time many of the clinically healthy rats showed demyelinating lesions which were located at the typical predilection sites of SDE. These observations indicated that SDE was preceded by clinically silent AE lesions.
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PMID:Sequence of murine coronavirus JHM induced neuropathological changes in rats. 633 Jun 3

Infection of rats with the murine coronavirus JHM led to acute or subacute encephalitis. Viral and host factors greatly influenced the outcome of the infection. A number of temperature-sensitive (ts) mutants was obtained which differed widely in their capacity to induce lesions of the central nervous system (CNS) in rats. Under defined conditions a subacute demyelinating encephalomyelitis ( SDE ) with pronounced clinical signs was observed 14-160 days post infection (p.i.). A number of rats, which showed a remission of SDE later developed a relapse of the disease accompanied by neurological symptoms. Neuropathological examination of such animals revealed lesions of active demyelination and extended remyelinated areas. The presence of viral antigen or infectious virus in the CNS of these rats demonstrated that they were persistently infected. Further investigations indicated that this virus infection triggers a cell mediated immune response against basic myelin protein which may contribute to the development of subacute to chronic encephalomyelitides .
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PMID:Virological and immunological aspects of coronavirus induced subacute demyelinating encephalomyelitis in rats. 633 Nov 17

Disease induced by 3 virulent strains of Canine Distemper Virus (CDV) was compared in specific pathogen-free Beagle dogs. All strains produced an encephalomyelitis but variation was observed in the severity, clinical course and resulting neuropathology. Infection with Snyder Hill strain of CDV was consistently acute; dogs either succumbed 14 to 19 days post-inoculation (PI) or recovered. Lesions in the neuraxis were those of a polioencephalomyelitis. In contrast, CDV strain A75-17 produced subacute to chronic disease in which demyelination was the predominant finding. Some dogs succumbed, generally around 28 to 42 days PI. Total recovery was again recorded for some members of the group. Others developed persistent central nervous system (CNS) infection but remained clinically stable until electively killed with barbiturate, up to 62 days PI. CDV strain R252 also induced delayed, predominantly white matter disease with a mixed pattern of mortalities, persistent infections and recoveries, similar to A75-17. Neutralizing antibody responses correlated with the disease course. Dogs which died had low serum titres or lacked serum antibody. Recovering dogs had the earliest and highest titres. A few dogs with persistent CNS infection had antibody in the cerebrospinal fluid also. Current concepts of the pathogenesis of canine distemper encephalomyelitis (CDE) are discussed and a basis for the strain-dependent clinical and pathological expression of CDE is proposed. Viral strain appears to be an important factor in this common disease of the canine CNS.
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PMID:Canine distemper encephalomyelitis: variation with virus strain. 669 31

A Borna disease virus (BDV)-like agent was isolated from the central nervous system (CNS) of cats with a spontaneous non-suppurative encephalomyelitis ('staggering disease'). In contrast to the rabbit-adapted BDV strain V, which can be propagated in several primary and permanent cell cultures, the cat virus grew only in embryonic mink brain cells. Infection of adult Wistar rats with feline brain tissue material did not result in clinical disease during a period of 5 months, nor in growth of infectious virus in the brain. However, using the brain suspension of a newborn rat inoculated with feline brain tissue material, it was possible to induce typical Borna disease (BD) in four adult rats. This indicates a possible adaptation of the cat virus during passages in rats. By the use of an RT-PCR technique, BDV-specific RNA could be detected in a majority of brain samples from diseased cats. BDV-specific antigen was demonstrated in feline CNS samples both by immunohistochemistry and ELISA. However, the amount of BDV RNA and BDV antigen was less in the cats as compared to horses with BD, providing further support for the notion that a distinct feline BDV strain exists.
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PMID:Staggering disease in cats: isolation and characterization of the feline Borna disease virus. 756 58

The distribution, spread, neuropathology, tropism, and persistence of the neurovirulent GDVII strain of Theiler's virus in the central nervous system (CNS) was investigated in mice susceptible and resistant to chronic demyelinating infection with TO strains. Following intracerebral inoculation, the virus spread rapidly to specific areas of the CNS. There were, however, specific structures in which infection was consistently undetectable. Virus spread both between adjacent cell bodies and along neuronal pathways. The distribution of the infection was dependent on the site of inoculation. The majority of viral RNA-positive cells were neurons. Many astrocytes were also positive. Infection of both of these cell types was lytic. In contrast, viral RNA-positive oligodendrocytes were rare and were observed only in well-established areas of infection. The majority of oligodendrocytes in these areas were viral RNA negative and were often the major cell type remaining; however, occasional destruction of these cells was observed. No differences in any of the above parameters were observed between CBA and BALB/c mice, susceptible and resistant, respectively, to chronic CNS demyelinating infection with TO strains of Theiler's virus. By using Southern blot hybridization to detect reverse-transcribed PCR-amplified viral RNA sequences, no virus persistence could be detected in the CNS of immunized mice surviving infection with GDVII. In conclusion, the GDVII strain of Theiler's murine encephalomyelitis virus cannot persist in the CNS, but this is not consequent upon an inability to infect glial cells, including oligodendrocytes.
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PMID:The neurovirulent GDVII strain of Theiler's virus can replicate in glial cells. 763 6

Infection of the central nervous (CNS) system by the human immunodeficiency virus (HIV) depends on the migration of infected hematogenous cells into the brain. We thus used quantitative light and electron microscopic immunocytochemistry to study the homing and turnover of bone marrow derived cells in the CNS in radiation bone marrow chimeras under normal conditions and in experimental autoimmune encephalomyelitis (EAE) as an experimental model of brain inflammation. Our studies suggest the following conclusions. First, the central nervous system is continuously patrolled by a small number of T-lymphocytes and monocytes. Meningeal and perivascular monocytes are slowly replaced by hematogenous cells under normal conditions, and this turnover is accelerated in the course of inflammation. In contrast, resident microglia represent a very stable cell pool, which in adult animals is only exceptionally replaced by hematogenous cells, even after recovery from severe brain inflammation. Second, although in bone-marrow-chimeric animals resident microglia, astrocytes, and ependymal cells are not able to present antigen to Lewis T-lymphocytes, the inflammatory reaction in EAE is qualitatively and quantitatively similar in these animals compared to fully histocompatible Lewis rats. Finally, resident microglia express the macrophage activation antigen ED1. Thus, microglia cells appear to function as effector cells in EAE lesions.
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PMID:Bone marrow derived elements and resident microglia in brain inflammation. 767 81

Akabane virus, an arthropod-borne Bunyavirus, is the major cause of epizootics of congenital malformations in ruminants in Australia, Japan, Korea, and Israel, and is suspected to be a cause of sporadic outbreaks elsewhere. Blood-sucking insects, such as biting midges, transmit the virus horizontally to vertebrates. Climatic factors influence the seasonal activity and geographic range of the vector population and, therefore, occurrence of related disease. Inoculated ruminants seroconvert rapidly after a short subclinical viremia. Infection is of consequence only if ruminants are pregnant and not protected by adequate specific neutralizing antibodies. In naive pregnant animals, virus may spread hematogenously to replicate and persist in trophoblastic cells of placental cotyledons and subsequently invade the fetus. A distinct tropism for immature rapidly dividing cells of the fetal central nervous system and skeletal muscle results in direct virus-induced necrotizing encephalomyelitis and polymyositis. If fetuses survive, such injury may manifest as arthrogryposis, hydranencephaly, porencephaly, microencephaly, hydrocephalus, or encephalomyelitis at term. The earlier in gestation that fetal infection occurs, the more severe the lesions, reflecting the large population of vulnerable cells and lack of fetal immunocompetency at earlier stages of pregnancy. Injury during the period of critical cell migration and differentiation in organogenesis may substantially disrupt structural development in target organs. Late gestational infections cause nonsuppurative inflammation in the brain and spinal cord, premature birth, or fetal death with stillbirth or abortion. Affected neonates are nonviable. Control is by vaccination but is not always justified economically. Akabane viral infections must be differentiated from infections with other teratogenic viruses (including related Bunyaviruses), inherited conditions, and maternal intoxications. Diagnosis is made by serology and viral isolation.
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PMID:Akabane virus. 772 35

Infection with an avirulent strain of Semliki Forest virus (SFV-A7) facilitates the development of experimental allergic encephalomyelitis (EAE) in a genetically resistant BALB/c mouse strain. Irradiation which is necessary for EAE induction caused a decrease in the total number of lymphocytes and an increase in CD4+/CD8+ T cell ratio in the spleen of BALB/c mice. EAE induction increased the ratio further until clinical and histological signs of EAE appeared. Entry of perivascular CD4+ and CD8+ cells preceded the onset of clinical signs and the appearance of MAC-1+ cells in the central nervous system (CNS). In the acute phase of EAE, cellular infiltrates, which were sparse, consisted mainly of MAC-1+ cells and a few CD4+ and CD8+ cells. Inflammatory cells gradually disappeared during the recovery phase. SFV-A7 infection after irradiation and EAE induction did not significantly change the CD4+/CD8+ ratio in the spleen or in the CNS infiltrates but enhanced the entry of inflammatory cell into the CNS. Similar perivascular cell influx was also seen in untreated mice infected with SFV-A7. We conclude that observed rapid reduction of splenic mononuclear cells and increase of the CD4+/CD8+ T cell ratio caused by irradiation prior EAE induction are early crucial events in disease induction in this resistant strain of mice. SFV-A7 infection, which further facilitates the development of EAE, does not induce immunoregulatory changes but provides its effect by enhancing the entry of inflammatory cells into the CNS. The combination of these two mechanisms thus effectively breaks the natural resistance against EAE in this genetically resistant mouse strain.
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PMID:Facilitation of experimental allergic encephalomyelitis by irradiation and virus infection: role of inflammatory cells. 796 84


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