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)

Here we report a comparative analysis of interleukin-16 (IL-16) expression by microglial cells of the normal rat brain in trimethyltin (TMT) neurotoxicity, experimental autoimmune uveitis (EAU), encephalomyelitis (EAE), and viral infection (Borna disease, Borna disease virus) by immunohistochemistry. Striking differences were observed. In contrast to the human brain, IL-16 was not expressed constitutively in the rat brain. Remote activation of microglial cells of the optic tract in EAU did not result into IL-16 expression. TMT intoxication induced expression in microglial cells of the hippocampus. In EAE and BDV, massive IL-16(+) microglial cells could be seen. Thus, IL-16 is a descriptor of microglial cell activation that discriminates between different disease models, and might be a valuable marker for the detection of microglia activation in human and rat central nervous system (CNS) diseases.
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PMID:Expression of interleukin-16 by microglial cells in inflammatory, autoimmune, and degenerative lesions of the rat brain. 1469 45

This article presents the etiology, epidemiology, clinical features,and diagnosis of the primary viral neurologic diseases observed in ruminants. In general, these viral neurologic diseases are uncommon but often fatal. Rabies virus is perhaps the most important cause of encephalitis in cattle because of the public health implications. Other viral encephalitis diseases in ruminants include bovine herpesvirus encephalomyelitis, pseudorabies, malignant catarrhal fever, ovine and caprine lentiviral encephalitis, West Nile virus encephalitis, Borna disease, paramyxoviral sporadic bovine encephalomyelitis,and ovine encephalomyelitis (louping-ill).
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PMID:Viral diseases of the ruminant nervous system. 1520 29

An apparently novel neurological disease clinically characterized by shaking, tremors, seizures, staggering gait, and ataxia was first observed in farmed mink kits in Denmark in 2000 and subsequently in Sweden, Denmark, and Finland in 2001, and again in Denmark in 2002. Lymphoplasmacytic encephalomyelitis was found in the affected kits. The lesions were most severe in the brainstem and cerebellum and consisted of neuronal degeneration and necrosis, neuronophagia, focal and diffuse gliosis, perivascular cuffs formed by lymphocytes, plasma cells and macrophages, and segmental loss of Purkinje cells. Testing was conducted to determine the cause of the disease, including general virological investigations (virus culture, negative-staining electron microscopy, immunoelectron microscopy, polymerase chain reaction for herpesviruses, adenoviruses, pestiviruses, and coronaviruses), tests for specific viral diseases (canine distemper, Borna disease, Louping ill, West Nile virus infection, tick-borne encephalitis, Aleutian disease), tests for protozoa (Toxoplasma gondii, Neospora caninum, Encephalitozoon cuniculi), bacteria (general culture, listeria, Clamydophila psittaci), and intracerebral inoculation of neonatal mice. The results of all these investigations were negative. One group of 3 mink kits inoculated intracerebrally with brain homogenate of affected mink developed clinical signs and histological lesions similar to those observed in naturally infected mink. Based on the histopathological features, it is postulated that the disease is caused by a yet unidentified virus.
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PMID:Investigations into shaking mink syndrome: an encephalomyelitis of unknown cause in farmed mink (Mustela vison) kits in Scandinavia. 1530 41

Greyhound meningoencephalitis is currently classified as a breed-associated idiopathic central nervous system inflammatory disorder. The non-suppurative inflammatory response can be distinguished from the other breed-associated disorders based on histopathology and lesion topography, however the nature of the response primarily suggests a viral infection. In the present study PCR and RT-PCR technologies were employed on frozen cerebral tissue from confirmed cases of meningoencephalitis to target specific viruses and protozoa likely to be implicated and to exclude the presence of bacterial 16SrRNA. Secondly, degenerate primers were used to detect viruses of the herpesvirus and flavivirus families. In addition cerebral tissues were probed for West Nile Virus. Viral nucleic acid sequences to Borna disease virus, to louping ill, tick borne encephalitis, West Nile and other flaviviruses were not detected. Canine distemper virus was detected in one animal with 97% homology to strain A75/15. Degenerate PCR for herpesviruses detected viral amplification products in one animal with 90% homology to canine herpesvirus DNA polymerase gene. Protozoal amplification products were only detected in a single dog with pathological confirmation of a combination of lesions of greyhound meningoencephalitis and a protozoal encephalomyelitis. Neospora was confirmed with sequence homology to Austrian strain 1. Bacterial 16SrRNA was not detected. The present study supports previous observations that many of the known microbial causes of canine meningoencephalitis are not involved. Findings could reflect that the causal agent was not specifically targeted for detection, or that the agent is at undetectable levels or has been eliminated from brain tissue. The potential roles of genetics and of molecular mimicry also cannot be discounted.
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PMID:Greyhound meningoencephalitis: PCR-based detection methods highlight an absence of the most likely primary inducing agents. 1696 61

Borna disease virus (BDV) is a neurotropic virus that causes a persistent infection in the central nervous system (CNS) of many vertebrate species. Although a severe reactive gliosis is observed in experimentally BDV-infected rat brains, little is known about the glial reactions contributing to the viral persistence and immune modulation in the CNS. In this regard, we examined the expression of an astrocyte-derived factor, S100B, in the brains of Lewis rats persistently infected with BDV. S100B is a Ca(2+)-binding protein produced mainly by astrocytes. A prominent role of this protein appears to be the promotion of vascular inflammatory responses through interaction with the receptor for advanced glycation end products (RAGE). Here we show that the expression of S100B is significantly reduced in BDV-infected brains despite severe astrocytosis with increased glial fibrillary acidic protein immunoreactivity. Interestingly, no upregulation of the expression of S100B, or RAGE, was observed in the persistently infected brains even when incited with several inflammatory stimuli, including lipopolysaccharide. In addition, expression of the vascular cell adhesion molecule 1 (VCAM-1), as well as the infiltration of encephalitogenic T cells, was significantly reduced in persistently infected brains in which an experimental autoimmune encephalomyelitis was induced by immunization with myelin-basic protein. Furthermore, we demonstrated that the continuous activation of S100B in the brain may be necessary for the progression of vascular immune responses in neonatally infected rat brains. Our results suggested that BDV infection may impair astrocyte functions via a downregulation of S100B expression, leading to the maintenance of a persistent infection.
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PMID:Downregulation of an astrocyte-derived inflammatory protein, S100B, reduces vascular inflammatory responses in brains persistently infected with Borna disease virus. 1737 96

The virus of equine encephalomyelitis (eastern strain) evokes in the horse, calf, sheep and dog an unusually intense encephalomyelitis characterized by acute primary degeneration of nerve cells, the appearance in neurons of the brain stem and elsewhere of nuclear inclusions resembling those in Borna disease and poliomyelitis, polymorphonuclear infiltration in the nervous tissues with early microglial proliferation, and perivascular cuffing with mononuclears and polymorphonuclears in varying proportions. The grey matter is affected more than the white. Lesions may be less marked in the striatum, brain stem and cord than in the cerebral cortex, thalamus and hypothalamic region, and are always of low grade in the cerebellum. Meningeal infiltration is secondary. Similar changes produced in the horse by the western strain of virus are less intense and extensive. In the guinea pig, rabbit and mouse, the eastern virus causes an acute encephalomyelitis which, as is usual in neurotropic virus diseases of these lowly species, has a special tendency to affect the higher olfactory centers. In addition to inclusions in the nerve cells, tiny oxyphilic bodies occur with less frequency in the glial and mesodermal nuclei of the guinea pig. In this animal, too, interstitial or bronchopneumonia may complicate the picture. In the guinea pig the disease resulting from infection with the western virus may be indistinguishable from that due to the eastern.
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PMID:THE HISTOLOGY OF EQUINE ENCEPHALOMYELITIS. 1987 Feb 64

Thanks to new technologies which enable rapid and unbiased screening for viral nucleic acids in clinical specimens, an impressive number of previously unknown viruses have recently been discovered. Two research groups independently identified a novel negative-strand RNA virus, now designated avian bornavirus (ABV), in parrots with proventricular dilatation disease (PDD), a severe lymphoplasmacytic ganglioneuritis of the gastrointestinal tract of psittacine birds that is frequently accompanied by encephalomyelitis. Since its discovery, ABV has been detected worldwide in many captive parrots and in one canary with PDD. ABV induced a PDD-like disease in experimentally infected cockatiels, strongly suggesting that ABV is highly pathogenic in psittacine birds. Until the discovery of ABV, the Bornaviridae family consisted of a single species, classical Borna disease virus (BDV), which is the causative agent of a progressive neurological disorder that affects primarily horses, sheep, and some other farm animals in central Europe. Although ABV and BDV share many biological features, there exist several interesting differences, which are discussed in this review.
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PMID:Avian bornavirus associated with fatal disease in psittacine birds. 2021 10


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