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

Colonial bats (Myotis supp. and Eptesicus sp.) were infected with eastern equine encephalomyelitis virus by subcutaneous inoculation or by the bite of infected mosquitoes. Bats were maintained in an environment simulating conditions encountered in hibernacula or in summer maternal colonies. Virus was detected in the blood of hibernating bats at irregular intervals over a 42-day observation period; viremia perhaps was influenced by the amount of disturbance (arousal) involved in the blood sampling process. Target organs included brown fat, spleen, lung, kidneys, pancreas, and liver. Neutralizing antibody was not detected in sera collected from these bats between days 4 and 42 post-inoculation. In nonhibernating bats, virus was recovered from mammary glands, brown fat, pancreas, lungs, kidneys, and liver, in addition to blood. Attempts to infect bats orally or to transmit virus to suckling mice by the bite of viremic bats were unsuccessful. Virus was transmitted from viremic chickens to E. fuscus by the bite of Culiseta melanura and Aedes aegypti.
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PMID:Eastern equine encephalomyelitis virus in experimentally infected bats. 4 Nov 9

Fluorescent antibody study showed persistent infection of egg-adapted avian encephalomyelitis virus in the central nervous system and pancreatic tissues of infected embryos and chickens hatched from them. The limited organ tropism of the egg-adapted virus in hatched chickens was in striking contrast to the systemic infection that occurs with a field strain. In chidkens orally infected with egg-adapted virus strains, transient infection of a few organs was found despite occurrence of viremia.
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PMID:Immunofluorescent study on egg-adapted avian encephalomyelitis virus infection in chickens. 20 77

A serial 34-chicken pancreas passage of avian encephalomyelitis virus by oral administration was successful. Oral inoculation test with 4 passaged viruses showed rapid infection of the duodenal wall and unchangeable infection of pancreas diminishing the viral invasiveness to other organs. The passaged virus caused neither detectable viremia nor clinical avian encephalomyelitis signs and produced neutralizing antibody of high titers.
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PMID:Pancreas-passaged avian encephalomyelitis virus and its immunogenicity. 20 48

An association was demonstrated between the development of clinical infectious avian encephalomyelitis (IAE), the persistence and titre of infectious avian encephalomyelitis virus (IAEV) in the brain of the chicken, the duration of detectable viraemia and the age of the chicken at the time of infection with the virus. The older the chicken at the time of infection the milder the disease, the lower the virus titre in the brain and the shorter the period of viraemia. IAEV serum neutralising antibody was produced earlier after infection in older chickens, and its detection was associated with decreasing virus titres in the brain and the cessation of detectable viraemia. Treatment of chickens with testosterone in ova, to inhibit the development of antibody synthesis, prevented the onset of age-associated resistance and testosterone treated birds were as susceptible to clinical IAE as baby chickens. The results suggested that the ability to produce IAEV serum neutralising antibody was an important component of age-associated resistance to IAE.
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PMID:The pathogenesis of infectious avian encephalomyelitis. 3. The relationship between viraemia, invasion of the brain by the virus, and the development of specific serum neutralising antibody. 20 59

The epizootic Trinidad donkey strain of Venezuelan equime encephalomyelitis virus (VEE) was cleared slowly from the circulation of rhesus monkeys following intravenous inoculation, while the live, attenuated vaccine strain, TC-83, was cleared rapidly. The efficent clearance of TC-83 vaccine may be a factor in the lower viremia and benign course of TC-83 virus infection in rhesus monkeys.
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PMID:Vascular clearance of venezuelan equine encephalomyelitis viruses as a correlate to virulence for rhesus monkeys. 41 57

During a 2-year observation of white rats and guinea pigs infected with human acute encephalomyelitis virus a typical picture of the disease was observed with exacerbations and remissions quite characteristic of chronic forms of multiple encephalomyelitis and multiple sclerosis of man. The presence of the virus in animals and marked pathomorphological lesions in the central nervous system were shown not to prevent remissions. The evidence of association of chronic infection with long-term viremia is also important.
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PMID:[Chronic encephalomyelitis in white rats and guinea pigs]. 100 17

Study of viremia in susceptible experimental animals showed all the blood fractions to take part in the infectious process both in acute diseases and in the chronic course of infections caused by various neuroviruses. Thus in animals infected with human acute encephalomyelitis, tick-borne encephalitis, lymphocytic choriomeningitis viruses viremia was observed throughout the entire short period of infection terminating fatally, as a rule. In such cases viremia was of a mixed character, the viruses being found in all blood fractions. The intensity of viremia and the degree of involvement of plasm and blood cell elements into the infectious process may depend upon the animal species, virus strains, form of the disease (acute, chronic). In chronic encephalomyelitis in rats and guinea pigs infected with human acute encephalomyelitis virus viremia are observed for two years (the observation period). In chronic encephalomyelitis blood cells were more actively involved in the infectious process. Virus was found in leukocytes and erythrocytes more frequently than in plasm, though the total amount of virus in the blood was much lower than that in the acute form of this disease. Sequential multiple passages of AEM virus from the blood to the brain in experiments with some strains resulted in intensive viremia thereby demonstrating the possibility of AEM adaptation to the blood tissue.
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PMID:[Study of viremia in experimental neuroviral infections]. 122 Feb 45

Three calves (Nos. 1, 2 = 7 days old; No. 3 = 21 days old) were inoculated subcutaneously with virulent Rift Valley fever (RVF) virus. All calves became viremic and clinically ill, but the two 7-day-old calves were moribund and were euthanatized subsequently on post-inoculation day (PID) 3. Highest viral titers were measured in the serum, with lesser concentrations in the brain, heart, spleen, and liver of these animals. Viral antigens were detected by immunohistochemical analysis only in the livers, where positive staining was localized in coalescing foci of hepatocellular necrosis. The 21-day-old calf appeared to recover after viremia and pyrexia but became lethargic and ataxic and was euthanatized on PID 9. The calf was no longer viremic, and RVF virus was isolated only from the brain. Microscopic examination of the central nervous system revealed diffuse perivascular infiltrates of lymphocytes and macrophages, multifocal meningitis, and focal areas of neuronal necrosis and aggregates of macrophages, lymphocytes, and neutrophils throughout all regions of the brain and cervical spinal cord. There was positive immunohistochemical staining for viral antigens within the cytoplasm of neurons and glial cells throughout the central nervous system. Thus, RVF virus can cause encephalomyelitis in calves, and the specific virologic diagnosis can be made by immunohistochemical localization of viral antigens in formalin-fixed tissues.
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PMID:Rift Valley fever virus-induced encephalomyelitis and hepatitis in calves. 144 95

Infection of female BALB/c mice with encephalomyocarditis virus results in the development of a paralytic syndrome in 7 to 10 days postinoculation. Previous studies had suggested the involvement of an immune component in the development of central nervous system pathology. We have examined the effects of T-cell depletion on the development of polioencephalitis (neuronal necrosis and inflammation of the brain and brain stem) and the relative contribution of the CD4+ and CD8+ subsets following the establishment of viremia. We show that monoclonal antibody depletion of T cells is effective in the reduction of polioencephalitis when given prior to viral inoculation. However, administration of the antibodies 12 h or more after viral inoculation failed to alter the development of polioencephalitis or encephalomyelitis. We conclude that T cells are involved in the development of central nervous system disease during the initial stages of infection but are not responsible for the later progression of disease.
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PMID:Indirect role of T cells in development of polioencephalitis and encephalomyelitis induced by encephalomyocarditis virus. 167 48

Eighteen equids were inoculated with eastern equine encephalomyelitis (EEE) and 18 equids with western equine encephalomyelitis (WEE) viruses to produce EEE virus- and WEE virus-immunized equids. Twelve surviving EEE virus-seropositive equids, 15 surviving WEE virus-seropositive equids, and 10 nonimmunized, seronegative equids (controls) were subsequently inoculated with an equine pathogenic (epizootic) strain of Venezuelan equine encephalomyelitis (VEE) virus to determine cross-protective immunity. Challenge infection produced 90% mortality in control (nonimmunized) equids, and 40% mortality in WEE virus-seropositive equids; all EEE virus-seropositive equids survived. Postchallenge exposure VEE viremia levels in EEE virus- or WEE virus-seropositive equids were lower than those in the 10 nonimmunized VEE virus-inoculated control equids. Plaque-neutralizing antibody responses to VEE virus in the EEE virus- and WEE virus-seropositive equids were similar in time of onset and titer to the antibody responses of nonimmunized equids. Neutralizing antibody to the third equine encephalomyelitis virus (either EEE virus or WEE virus) was detectable in 19 of 27 equids after inoculation with the challenge virus, VEE. Demonstration of cross-protective immunity between EEE or WEE virus and VEE virus in equids confirmed field observations made during the VEE epizootic in Texas in 1971.
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PMID:Cross-protective immunity between equine encephalomyelitis viruses in equids. 255 75


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