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

The E variant of encephalomyocarditis (EMC) virus causes an encephalomyelitis and coagulative necrosis of the pancreas and parotid glands in some but not all strains of inbred and outbred mice. In other models of disease caused by picornaviruses, depletion of specific lymphocyte subsets abrogates the development of tissue lesions. In this study, severe encephalomyelitis and acinar pancreatitis and parotitis developed in adult male A/J mice infected with 100 PFU of EMC virus. Depletion of the CD4+ subset of T lymphocytes in vivo with a monoclonal antibody (MAb) prior to EMC virus inoculation protects mice from developing encephalomyelitis, pancreatitis, and parotitis. This effect is also seen when animals are treated with anti-CD4 and anti-CD8 in combination, but the anti-CD8 MAb alone does not ameliorate the disease. Overall, concentrations of virus in tissues from anti-CD4-treated animals are lower than in immunologically intact control mice. Small-plaque variants of virus were also recovered from the tissues in some animals in this group. CD4+ lymphocytes are involved in the expression of EMC virus-induced pancreatitis and parotitis in A/J mice. This specific subset of T cells would appear to influence EMC viral tropism or replication in various organs.
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PMID:Immunomodulation of encephalomyocarditis virus-induced disease in A/J mice. 170 84

Camostat mesilate (FOY305), a synthetic serine protease inhibitor and has been developed as a drug for pancreatitis, is effective in suppressing acute experimental allergic encephalomyelitis in Lewis rats. Loss of weight, clinical score and yield of myelin protein from brain stem were improved by daily injection of FOY305 compared with saline from day 6 after inoculation with homogenate of guinea pig spinal cord. A significant decrease of yield of myelin has been shown here for the first time in acute EAE in Lewis rat. This is in accord with myelin breakdown demonstrated morphologically. Our study also demonstrates a significant improvement of yield of myelin protein by FOY305. Our results suggest the possibility of a clinical application of this protease inhibitor for human demyelinating diseases such as multiple sclerosis.
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PMID:Suppressive effect of camostat mesilate (FOY 305) on acute experimental allergic encephalomyelitis (EAE). 245 35

A study of the clinical and pathological changes in pigeons experimentally inoculated with a herpesvirus isolated recently from natural cases of a condition termed contagious paralysis was carried out. Signs and pathological findings similar to those recorded in natural cases were produced after inoculation of the isolate via different routes. The incubation period differed according to the route of inoculation from 2 to 10 days and the course of the disease from 5 to 21 days. The mortality ranged from 100% in the intracerebrally inoculated pigeons to 61% in the orally infected ones. The clinical signs and the gross and histopathological changes included mainly progressive paralysis, meningo-encephalomyelitis, pancreatitis and sometimes enteritis.
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PMID:Experimental study of contagious paralysis of pigeons. 626 60

A case of progressive encephalomyelitis with rigidity (PEWR) associated with hepatitis C virus (HCV) is reported. A 58 year-old woman presented with a clinical picture of progressive quadriparesis, sensory loss, sphincter dysfunction, painful muscle spasms in the upper and lower limbs and continuous muscle unit activity in electromyography. She developed hepatitis, pancreatitis and HCV-RNA was detected in the plasma by reverse transcription-polymerase chain reaction (RT-PCR). Postmortem histopathological examination showed encephalomyelitis with perivascular lymphocyte cuffing, infiltration and neuronal loss mainly affecting the brainstem and cervical spinal cord. The RT-PCR analysis of the postmortem brain, brainstem, liver, pancreas, plasma and CSF samples revealed the presence of HCV genome in all specimens except CSF. Clinical features, postmortem histopathology and PCR results and the possible etiopathogenesis of PEWR are briefly discussed.
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PMID:PCR detected hepatitis C virus genome in the brain of a case with progressive encephalomyelitis with rigidity. 908 76

The pathological and immunohistochemical findings of avian encephalomyelitis (AE) were described in various tissues of naturally infected pigeons of a flock from a outbreak in Turkey. Clinically, paresis, paralysis, circling movement and torticollis of the head associated with nervous signs were marked symptoms among the diseased pigeons. At necropsy, small or large white-greyish foci were detected in the pancreas, and erosive-ulcerative foci along with petechial hemorrhages in ingluves. Histopathologically, lesions in central nervous system, particularly in the cerebellum molecular layer, consisted of non-suppurative encephalomyelitis. Lesions in the pancreas revealed non-suppurative pancreatitis along with acinar degeneration and necrosis and/or lymphoid aggregations. Immunohistochemical staining of formalin-fixed, paraffin-embedded tissues was performed using a direct-fluorescein antibody technique with chicken anti-AE virus serum fluorescein isothiocyanate conjugate. Viral antigen was strongly stained in cytoplasm of epithelial cells of the exocrine glands, and neurons of the cerebral hemispheres and midbrain. In addition, viral antigen was also marked in the kidneys and tissues of the digestive system. Consequently, this article is, to our knowledge, the first report of natural AE in pigeons.
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PMID:Avian encephalomyelitis in naturally infected pigeons in Turkey. 1522 70

1. A viral agent, Powers, causing myocarditis, adipositis, pancreatitis, hepatitis, and encephalomyelitis but not myositis in suckling mice 1 to 2 days old has been isolated from the stool of a patient in whom the clinical diagnosis was "non-paralytic poliomyelitis." 2. Serological evidence linking the virus to the clinical disease observed was clear only in the case of "non-paralytic poliomyelitis" from which it was isolated. 3. The possible relation of this agent to the Coxsackie group of viruses is discussed. No serological relationship with the Connecticut 5, Ohio R, and High Point strains was demonstrated. 4. A second virus, Matulaitis, has been isolated from a concurrent case of "non-paralytic poliomyelitis" in the same area. Lesions produced in infant mice by the two agents show certain differences.
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PMID:A viral agent isolated from a case of "non-paralytic poliomyelitis" and pathogenic for suckling mice: its possible relation to the coxsackie group of viruses. 1542 84

Enteroviral diseases are widespread and impose significant importance in medicine. Although the outcome of diseases that are associated with enteroviruses such as myocarditis, pancreatitis, hepatitis, or encephalomyelitis might be fatal, no specific antiviral therapy is yet available. We and others have shown that RNA interference (RNAi) effectively limits picornaviral replication and cytopathogenicity and improves survival in susceptible mice. However, little is known about the dependence of short interfering RNA (siRNA) efficacy on target region selection and emergence of viral escape mutants that may limit the effect of RNAi. The results of our study indicate that antiviral siRNA should be targeted preferentially to nonstructural protein coding regions because siRNA efficacy was consistently found to be superior compared to noncoding or structural protein coding regions. Further more, emergence of viral escape mutants that harbor single point mutations in the central part of the siRNA binding motif are the major factor that limits early therapeutic siRNA efficacy. The appearance of viral escape mutants can be sufficiently suppressed by combined administration of at least three distinct siRNA molecules. Therefore, genomic target selection and viral escape mutants are the most critical factors that limit early RNAi directed against enteroviral genomes. Both obstacles can be circumvented by appropriate target selection and combined siRNA administration.
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PMID:Anti-coxsackieviral efficacy of RNA interference is highly dependent on genomic target selection and emergence of escape mutants. 1746 62

The results of pathological, virological and polymerase chain reaction examinations carried out on 35 mute swans (Cygnus olor) that succumbed to a highly pathogenic avian influenza virus (H5N1) infection during an outbreak in Southern Hungary are reported. The most frequently observed macroscopic lesions included: haemorrhages under the epicardium, in the proventricular and duodenal mucosa and pancreas; focal necrosis in the pancreas; myocardial degeneration; acute mucous enteritis; congestion of the spleen and lung, and the accumulation of sero-mucinous exudate in the body cavity. Histopathological lesions comprised: lymphocytic meningo-encephalomyelitis accompanied by gliosis and occasional perivascular haemorrhages; multi-focal myocardial necrosis with lympho-histiocytic infiltration; pancreatitis with focal necrosis; acute desquamative mucous enteritis; lung congestion and oedema; oedema of the tracheal mucosa and, in young birds, the atrophy of the bursa of Fabricius as a result of lymphocyte depletion and apoptosis. The observed lesions and the moderate to good body conditions were compatible with findings in acute highly pathogenic avian influenza infections of other bird species reported in the literature. Skin lesions and lesions typical for infections caused by strains of lower pathogenicity (low pathogenic avian influenza virus) such as emaciation or fibrinous changes in the reproductive and respiratory organs, sinuses and airsacs were not observed. The H5N1 subtype avian influenza virus was isolated in embryonated fowl eggs from all cases and it was identified by classical and molecular virological methods.
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PMID:Pathobiology of highly pathogenic avian influenza virus (H5N1) infection in mute swans (Cygnus olor). 1749 39

A February 2015 outbreak of highly pathogenic avian influenza (HPAI) H5N8 in a flock of commercial Pekin ducks ( Anas platyrhynchos domesticus) in California was investigated in detail. Approximately 17,349 five-wk-old ducks experienced an increased mortality from a normal of eight birds per day to 24, 18, 24, 33, and 61 birds per day, respectively, in the last 5 days prior to flock depopulation. Clinically, there was decreased water and feed consumption, and approximately 1.0% of the affected flock exhibited neurologic signs. Necropsy of five clinically ill ducks revealed pale, patchy areas on the epicardium in two birds, pale foci of necrosis in the liver of one bird, and airsacculitis in three birds. Histopathology revealed multifocal nonsuppurative encephalomyelitis, myocarditis, myositis, pancreatitis, hepatitis, and glossitis. Immunohistochemistry revealed avian influenza virus (AIV) nucleoprotein in the nucleus and cytoplasm of various cells in the aforementioned organs, as well as in the skin and feathers. Eight of the 10 sera samples tested were positive for avian influenza antibodies by agar gel immunodiffusion serology. Oropharyngeal and cloacal swabs taken from 15 birds, as well as from the lungs, livers, pancreas, and spleen, were positive for AIV by real-time reverse transcriptase (rRT) PCR. AIV was isolated and typed as Eurasian lineage HPAI H5N8, clade 2.3.4.4, by the National Veterinary Services Laboratory, Ames, IA. Extensive surveillance of birds for AIV around the 10-km zone did not reveal any additional cases. Ducks on the affected premises were humanely euthanatized by foam and composted in-house, the houses were heated to 57 C for 4 days, and swabs were taken periodically from the compost to ensure negativity for AIV by rRT-PCR. The compost and litter were then removed, and the house was pressure cleaned, disinfected, and repopulated approximately 120 days after euthanatization of the ducks.
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PMID:Study of an Outbreak of Highly Pathogenic Avian Influenza H5N8 in Commercial Pekin Ducks ( Anas platyrhynchos domesticus) in California. 2962 Apr 70