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

The authors have investigated the spread of fixed and street strains of rabies virus from the site of injection to the central nervous system and salivary glands in various animal species. The results indicate conclusively that rabies virus is ordinarily transmitted from the site of exposure to the central nervous system via the peripheral nerves but that other than nerve transmission may occur in young animals, in highly susceptible species or in animals whose resistance has been altered by trauma or shock. Air-borne infection is occasionally possible. Blood-borne infection in nature is believed to be exceptional and less likely to occur in man, whose resistance to rabies is high, than in animals of species known to be highly susceptible. Evidence of nerve-borne transmission was also observed with herpes simplex virus but not with lymphocytic choriomeningitis virus or the GD7 and FA strains of mouse encephalomyelitis virus.
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PMID:PATHOGENESIS OF RABIES. 1410 54

A prolongation in the lives of Swiss mice inoculated intracerebrally with lymphocytic choriomeningitis virus (LCM) was observed after treatment with 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU). A variety of treatment schedules, including therapy once or twice daily up to 17 days and single treatments at various times after virus inoculation, were employed. Virus titers ranging to greater than 10(4) were detected in the blood and brains of surviving drug-treated animals. In three comparative studies in which different treatment schedules were used, BCNU was shown to exert a protective effect approximately equal to that of methotrexate in LCM virus-infected mice. Tests were also carried out to investigate the activity of BCNU in mice experimentally infected with eastern equine encephalomyelitis (EEE) virus, western equine encephalomyelitis virus, Semliki Forest (SF) virus, herpes simplex virus, influenza virus strain PR8, vaccinia virus strain WR, Rous sarcoma virus, Friend leukemia virus (FLV), and poliovirus. Slight increases in life span were observed in the treated EEE, SF, and influenza PR8 virus-infected animals. Significant reduction in splenomegaly in FLV-infected animals treated with BCNU was demonstrated. The possible mechanisms of LCM virus inhibition by BCNU, on the basis of these and other studies, were postulated to be either specific antiviral activity or inhibition of "lethal" immune response to the LCM virus. Each of these postulates is discussed.
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PMID:IN VIVO ANTIVIRAL ACTIVITY OF 1,3-BIS(2-CHLOROETHYL)-1-NITROSOUREA. 1433 66

Studies on island populations of house mice (Mus domesticus) and their viruses reveal insights into viral persistence in isolated communities. We surveyed the ectoparasites, endoparasites, and antiviral antibodies for 11 murine viruses and two bacteria of house mice inhabiting two islands off Australia. House mice on Boullanger Island were seropositive to two viruses, murine cytomegalovirus and epizootic diarrhea of infant mice. On subantarctic Macquarie Island, house mice were seropositive for five viruses: murine cytomegalovirus, lymphocytic choriomeningitis virus, mouse parvovirus, epizootic diarrhea of infant mice, and Theiler's murine encephalomyelitis virus. The diversity of antiviral antibodies was lower among populations of house mice on islands than those inhabiting mainland Australia. The decreased diversity of viruses in island populations of house mice may be a function of which agent the founder mice transfer to the island and related to the low densities which the host population may periodically reach over time.
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PMID:Pathogens of house mice on arid Boullanger Island and subantarctic Macquarie Island, Australia. 1473 70

Mitogen-activated protein (MAP) kinases are essential regulators in immune responses, and their activities are modulated by kinases and phosphatases. MAP kinase phosphatase (MKP) is a family of dual-specificity phosphatases whose function is evolutionarily conserved. A number of mammalian MKPs have been identified so far, but their specific physiological functions in negative regulation of MAP kinases have not been genetically defined. Here we examine innate and adaptive immune responses in the absence of MKP5. JNK activity was selectively increased in Mkp5 (also known as Dusp10)-deficient mouse cells. Mkp5-deficient cells produced greatly enhanced levels of pro-inflammatory cytokines during innate immune responses and exhibited greater T-cell activation than their wild-type counterparts. However, Mkp5-deficient T cells proliferated poorly upon activation, which resulted in increased resistance to experimental autoimmune encephalomyelitis. By contrast, Mkp5-deficient CD4(+) and CD8(+) effector T cells produced significantly increased levels of cytokines compared with wild-type cells, which led to much more robust and rapidly fatal immune responses to secondary infection with lymphocytic choriomeningitis virus. Therefore, MKP5 has a principal function in both innate and adaptive immune responses, and represents a novel target for therapeutic intervention of immune diseases.
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PMID:Regulation of innate and adaptive immune responses by MAP kinase phosphatase 5. 1530 13

A study has been made of the local effects following intramuscular injection of various neurotropic viruses. Early massive necrosis of muscle fibers accompanied by edema and acute inflammatory reaction is produced by Jungeblut's SK virus even in low concentrations. Similar but more slowly developing lesions follow the introduction of mouse encephalomyelitis GD-VII and FA strains. Strain 4727 (TO type) produces inflammatory changes with fibrosis in the intermuscular septa and necrosis of scattered individual fibers. The relatively avirulent FV strain (TO type) was not pathogenic for skeletal muscle. The Mitchell strain of lymphocytic choriomeningitis virus gives rise to a profuse lymphocytic and monocytic infiltration of the fat and connective tissue but does not cause necrosis of muscle fibers. No significant lesions resulted from intramuscular injection of the murine-adapted human poliomyelitis Lansing virus, the HF strain of herpes, a strain of Eastern equine encephalitis virus, or a still unidentified demyelinating mouse virus. Evidence is presented that the mouse encephalomyelitis virus GD-VII and Jungeblut's SK virus multiply locally in the injected limb. The GD-VII virus has been passed through four muscle to muscle passages and muscle lesions have been elicited at the same time. Specific and complete protection against myositis was obtained by anti-GD-VII and anti-SK rabbit sera.
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PMID:Myositis in mice following intramuscular injection of viruses of the mouse encephalomyelitis group and of certain other neurotropic viruses. 1809 66

Tick-borne borreliosis (Borrelia burgdorferi) is a common and complex disorder affecting the skin, the joints and the nervous system. It progresses through different clinical stages. The clinical spectrum of neuroborreliosis has expanded since the introduction and widespread application of specific serological tests. We have investigated 41 patients with Bannwarth's meningopolyneuritis (MPN) as the classical form of neuroborreliosis, in a prospective (26 patients) and a retrospective (15 patients) study. When questioned, 19/41 patients reported a tick bite and only 15/41, erythema migrans as the characteristic early skin lesion. In 34/41 patients typical MPN characterized by painful radiculoneuritis and/or cranial neuritis, especially facial palsy, were seen. Among these, 3 had a complicated form with a progressive remitting relapsing course or focal central nervous system involvement (hemiparesis, cerebellar syndrome); 2 had mild meningitis and facial nerve palsy bilaterally without radicular pain; and in 5 radicular pain was the only symptom. MPN associated with Lyme arthritis was observed only once. In 2 patients in the retrospective study (no antibiotics in the acute stage) we saw a chronic spinal cord disorder with spastic paresis several years after uncomplicated MPN, accompanied in 1 of them by acrodermatitis chronica atrophicans (ACA), the typical late-onset borrelia-induced dermatosis. In the acute stage of the disease 40/41 patients had a cerebrospinal fluid (CSF) syndrome compatible with MPN (mononuclear pleocytosis, blood-brain barrier dysfunction, elevated IgG and/or oligoclonal bands). IgG antibody titers against borrelia antigen were elevated in all patients in the serum and in 21/30 also in the CSF. In all patients pain was an early and prominent symptom; the first symptoms are usually felt in the region of the tick bite or the erythema, initially as diffuse myalgia, arthralgia or pain in the connective tissue. In the further course the migrating pain becomes more radicular in character, without being limited to defined dermatomic areas or peripheral nerves. The intense, burning pain is characterized by exacerbation during the night. Peripherally and centrally acting analgesics have only minor effects. Often neurological deficits are still absent at this time. Erythema migrans with radicular pain in the region of the dermatological lesion was observed in 2 patients. This is an early manifestation of MPN. After MPN and/or Lyme arthritis a sympathetic reflex dystrophy (SRD) developed in 2 patients. In a further patient SRD was observed right at the beginning of the illness, immediately before MPN. There is a close clinical similarity between SRD and the acute stage of ACA. Therefore, borreliosis can be assumed to produce a painful skin dystrophy like SRD or ACA by direct injury to the sympathetic nerves even in the early clinical stage of the infection. The main conditions to be considered in the differential diagnosis are polymyalgia rheumatica; lumbar disk herniation; inflammatory radiculopathies of other origin (e.g. herpes zoster); painful neuropathies, including the diabetic thoraco-abdominal form; internal disorders of chest and abdomen with referred pain; lymphocytic meningitis of other origin, encephalomyelitis; and sympathetic reflex dystrophy. High-dose penicillin G i.v. is a potent analgesic in all patients with tick-borne neuroborreliosis.
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PMID:[Pain syndromes in tick-borne neuroborreliosis. Clinical aspects and differential diagnosis.]. 1841 56

Limited data are available on the pathogen status of contemporary rodent colonies in Taiwan. Here we summarized the rodent pathogen diagnostic records of the Taiwan National Laboratory Animal Center during a 4-y period that representing approximately 10% of the rodent colonies in Taiwan. Demand for pathogen diagnostic service increased continuously from 2004 to 2007, with a 20% increase each year. In 2007, more than 20% of the mouse colonies were positive for mouse parvovirus, mouse hepatitis virus, Theiler murine encephalomyelitis virus, and Mycoplasma pulmonis, with fewer colonies diagnosed as having infections of pneumonia virus of mice, mouse adenovirus, lymphocytic choriomeningitis virus, and reovirus. Almost 40% of tested rat colonies were positive for Mycoplasma pulmonis and rat parvovirus, with fewer colonies containing Kilham rat virus, sialodacryoadenitis virus, pneumonia virus of mice, Sendai virus, and Syphacia spp. These data provide a sound overall picture of the health status of mouse and rat colonies in Taiwan.
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PMID:Microbial contaminations of laboratory mice and rats in Taiwan from 2004 to 2007. 1965 46

A specific complement fixation test can be obtained in various central nervous system virus infections by using as antigens emulsions of infected brain tissue, freezing and thawing the brain emulsion, and then centrifuging it in an angle head centrifuge at 3500 R.P.M. for 1 hour. The method has proved reliable in the case of rabies, St. Louis encephalitis, Japanese B encephalitis, lymphocytic choriomeningitis, Eastern equine encephalomyelitis, Western equine encephalomyelitis, louping ill, and spontaneous encephalomyelitis of mice (Theiler's disease). The specificity of the reaction, regardless of the virus involved, requires different temperatures of inactivation of the sera according to animal species: 56 degrees C. for guinea pig, 60 degrees C. for mouse, and 65 degrees C. for rabbit and dog sera, all heated for 20 minutes. For human sera a temperature of inactivation of 60 degrees C. also for 20 minutes has been adopted; at this temperature the reaction is in general specific. Complement-fixing antibodies in high titre were found in the sera of rabbits, guinea pigs, mice, and dogs immunized with rabies virus. Complement-fixing antibodies were present in high titre in sera drawn from two persons 8 years after an attack of louping ill, from five persons 2(1/2) years after an attack of Eastern equine encephalomyelitis, and from two persons 2(1/2) years after Western equine encephalomyelitis. In cases of St. Louis encephalitis and lymphocytic choriomeningitis, complement-fixing antibodies have been found shortly following infection but not after long periods.
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PMID:THE COMPLEMENT FIXATION TEST IN THE DIAGNOSIS OF VIRUS INFECTIONS OF THE CENTRAL NERVOUS SYSTEM. 1987 Nov 44

The infection of cats by the virus of infectious feline agranulocytosis is followed by the production of specific neutralizing and protective antibodies, and recovery from the disease is associated with the development of solid immunity to reinfection. From the evidence presented it is obvious that the virus is not related to the viruses of hog cholera, lymphocytic choriomeningitis, fox encephalitis, vesicular stomatitis, the Western type of equine encephalomyelitis, herpes, and B virus infection.
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PMID:THE VIRUS OF INFECTIOUS FELINE AGRANULOCYTOSIS : II. IMMUNOLOGICAL RELATION TO OTHER VIRUSES. 1987 Dec 64

Wild rodents are a potential source for pathogen introduction into laboratory animal research facilities. A study was designed to assess wild mice found at our institution by infectious disease surveillance. Wild white-footed mice (Peromyscus leucopus) were captured with live capture traps placed in areas in which wild mice had been reported in several animal facilities. Captured animals were euthanized by inhalation of CO(2), blood was collected by cardiocentesis (n = 10), and necropsy was performed (n = 8). Serum samples were negative for antibodies to mouse parvovirus (types 1 and 2), mouse minute virus, Sendai virus, pneumonia virus of mice, mouse hepatitis virus, Theiler murine encephalomyelitis virus, reovirus, rotavirus, lymphocytic choriomeningitis virus, mouse adenovirus, ectromelia virus, K virus, cilia-associated respiratory bacillus, and Mycoplasma pulmonis. Of the 8 animals that were necropsied, pelt and cecal examinations were negative for ectoparasites and pinworms, respectively. Histopathologic examination of brain, heart, lungs, liver, kidney, spleen, stomach, and small intestine revealed bacteria morphologically compatible with Helicobacter spp. in the cecal and colonic glands and occasionally in the gastric lumen and pits. Mesenteric lymph nodes and feces from 8 of the animals were submitted for PCR analysis for the detection of mouse parvovirus, mouse minute virus, mouse hepatitis virus, and Helicobacter spp.; 7 of the samples were PCR-positive for Helicobacter spp. At this time, wild mice found in our animal facilities do not appear to be a significant source of common laboratory mouse viral pathogens. However, they are a potential source of Helicobacter infections.
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PMID:Helicobacter spp. in wild mice (Peromyscus leucopus) found in laboratory animal facilities. 1993 Aug 23


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