Cases reported "Rubella"

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1/12. Sequential follow up observations of a patient with rubella associated persistent arthritis.

    In 1985 a patient was described whose persistent polyarthritis was found to be aetiologically linked to rubella virus infection through the detection of repeated maximal synovial lymphocyte proliferative responses to rubella virus antigen and by isolation of rubella virus from her synovium. Follow up over the succeeding seven years has shown continuing chronic polyarthritis and persistent synovial lymphocyte responses to rubella virus antigen with the additional observation that she has a defective humoral immune response against rubella virus.
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2/12. Virus-specific and autoreactive T cell lines isolated from cerebrospinal fluid of a patient with chronic rubella panencephalitis.

    Using a recently described technique for expanding of human T lymphocyte populations from cerebrospinal fluid (CSF), we investigated the local cellular immune response in a patient with chronic rubella panencephalitis. A total of 328 T cell lines (TCLs) was established by seeding CSF cells at limiting dilution into histoplates in the presence of irradiated feeder cells and phytohemagglutinin (PHA)-containing conditioned medium. 80% of TCLs expressed the CD4 CD8-, 5% the CD4-CD8 phenotype and 15% of TCLs contained different proportions of CD4 and CD8 cells. Of 191 TCLs analyzed, 85 were cytotoxic, as shown by their lectin-dependent cytotoxicity against allogeneic uninfected target cells. Eight of them demonstrated specificity for the autologous, rubella virus-infected target cells. When tested for antigen-specific proliferative activity, 26 TCLs responded to rubella antigen, 16 TCLs reacted to myelin basic protein (MBP), four TCLs to proteolipid protein (PLP), four to galactocerebrosides and two to actin. Fourteen out of 16 MBP-specific TCLs also responded, to a minor degree, to rubella antigen and/or actin. The results showed that the persisting rubella infection had given rise to autoreactive T cells. Virus-induced autoreactivity to brain antigens may be an important pathogenetic mechanism in other chronic inflammatory disorders of the CNS.
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3/12. First trimester prenatal diagnosis of congenital rubella: a laboratory investigation.

    Acute primary maternal infection with rubella virus during pregnancy often, but not invariably, leads to the congenital rubella syndrome. Diagnosis by detection of virus specific IgM in the mother is not always possible, and in those cases in which IgM is detected the fetus has not necessarily also been infected. A method for direct, prenatal detection of fetal infection would allow more accurate early diagnosis of congenital rubella syndrome. In this study a case of suspected preconception rubella infection that was not referred until 14 weeks after the appearance of a rash was studied to determine whether a retrospective serological diagnosis of primary rubella could be made, and whether direct evidence of fetal infection could be obtained from a chorionic villus biopsy specimen by detecting virus specific antigens or ribonucleic acid (rna) sequences. Monoclonal antibodies and a cloned complementary deoxyribonucleic acid probe were used successfully to detect antigens to rubella virus antigens and rna sequences in the chorionic villus biopsy specimen, which was taken at 15 weeks' gestation. This method should serve as a new approach to the diagnosis of congenital rubella syndrome in utero.
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4/12. Intrahepatic lymphocyte subpopulations in acute hepatitis in an adult with rubella.

    Rubella accompanied by serum aminotransferase elevations occurred in a 24-yr-old man. liver biopsy showed ballooning degeneration and focal necrosis of liver cells, clumped kupffer cells, and infiltration of inflammatory cells, mainly of the mononuclear type. Most mononuclear cells in the liver were CD8-positive and CD16-negative cells (cytotoxic T cells) which were in broad contact with the surface of liver cells. Leu 7 (natural killer) cells were few and sporadic. HLA class I antigens were expressed on liver cell membrane. Although hepatic involvement in adult rubella is not generally recognized, it may have been the cause of this patient's liver injury. Thus, cytotoxic T cells may play a role in liver injury in acute rubella infections in adults.
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5/12. subacute sclerosing panencephalitis and multiple sclerosis: in vitro measles immunity and sensitization to myelin basic protein.

    Three children with subacute sclerosing panencephalitis (SSPE), 12 patients with multiple sclerosis (MS) and 12 healthy persons were studied by the macrophage migration inhibition factor (MIF) assay with measles and rubella antigens and with myelin basic protein. For the SSPE patients the mean migration indexes /- standard deviation were 44.1 /- 10.9 for measles antigen, 38.7 /- 12.3 for rubella antigen and 49.8 /- 25.7 for myelin basic protein; for the MS patients the indexes were 103.0 /- 10.6, 93.8 /- 15.0 and 89.3 /- 19.9; and for the healthy subjects the indexes were 68.8 /- 22.6, 77.7 /- 31.3 and 100.1 /- 6.5. The results of this study showed increased cellular immunity to measles and rubella in SSPE patients as compared with healthy persons, and absence of immunity to measles in MS patients. patients with MS showed hypersensitivity to myelin basic protein during clinical exacerbations that was not associated with changes in immunity to measles, whereas all SSPE patients showed a significant response regardless to stage of illness.
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6/12. rubella virus antigen in lymphocytes of patients with angioimmunoblastic lymphadenopathy (AIL).

    Lymph node sections from 14 patients with angioimmunoblastic lymphadenopathy (AIL) were incubated with fluorescein-labeled specific antiserum against rubella virus antigen. In lymphoid cells from 11 patients intracytoplasmic rubella antigen was demonstrated. The results support the idea of a persistent virus infection in AIL.
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7/12. Relapsing neurological disorder associated with rubella virus infection in two sisters.

    A disseminated relapsing neurological disorder presented simultaneously in two sisters. Encephalitic features were present in one case. The illness was associated with a significant increase in rubella specific IgM in both sisters. Despite the absence of a rubella rash, this increase would be compatible with a recent infection by the rubella virus as a basis for the illness, and the persistent elevation, with active antigenic stimulation. It is suggested that both patients might represent the clinical manifestations of perivenous demyelination caused by the rubella virus, which, in view of the relapsing nature of the illness, has progressed to plaque formation.
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8/12. Rubella arthritis in adults. Isolation of virus, cytology and other aspects of the synovial reaction.

    rubella virus was isolated from three consecutive samples of synovial fluid after 1 to 4 days of arthritis in adults with typical naturally acquired rubella. In the two samples suitably prepared, cells in the synovial fluid were mononuclear, with numerous monocytes and macrophages. Detailed studies in one case revealed a close similarity in all respects to the illness caused by ross river virus, another member of the togaviridae. Cells in the synovial exudate of this patient showed intense phagocytosis. A fine nodular cytoplasmic distribution of virus antigen was detected by immunofluorescence in 45% of the cells. There was no depletion of the complement components C'3 and C'4 in serum or synovial fluid, and no evidence of excessive immune complexes in the circulation or of immune-complex uptake by cells in the synovial exudate or intima. Synovial intima from the suprapatellar region merely showed slight hyperplasia without cellular infiltration, indicating that the lodgement of virus and the inflammatory cellular reaction to it can be confined to limited regions of the synovial lining, at least in the early stages.
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9/12. Altered blood group expression in a patient with congenital rubella infection.

    An infant with probable congenital rubella infection developed altered blood group expression. This was noted at 4 months of age. The child's blood was typed on seven separate occasions during the first 8 weeks of life as type A, but on repeat testing, her cells failed to agglutinate with anti-A and anti-A,B typing serum. The A antigen was present, however, because an eluate made after incubating her red cells with anti-A contained anti-A, and A antigen was demonstrated on buccal mucosa cells. Altered expression of blood group A (loss of agglutinability) has occurred previously only in association with hematologic malignancy.
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10/12. Desquamative interstitial pneumonia and antigen-antibody complexes in two infants with congenital rubella.

    Desquamative interstitial pneumonia was observed in two infants with the late-onset congenital rubella syndrome. In both infants this unusual lung disease was associated with circulating immunoglobulin m complexes and interstitial pulmonary deposits of IgM by immunofluorescence. Both infants had igg deficiency. The first child recovered with a reduction in IgM complex levels and synthesis of rubella-specific IgG. The second infant died during the acute phase of his illness at which time there were high serum concentrations of IgM complexes and slightly increased levels of IgG complexes. Delayed maturation of the immune response in congenital rubella may predispose to persistent antigenemia and pulmonary deposition of rubella antigen-containing IgM complexes resulting in an acute form of interstitial pneumonia.
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ranking = 3
keywords = antigen
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