Cases reported "Measles"

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1/26. Subacute measles encephalitis in a young man immunosuppressed for ankylosing spondylitis.

    Subacute measles encephalitis occurred 1 month after measles onset in a 26-year-old hiv-negative man undergoing immunosuppressive treatment for ankylosing spondylitis. He had seizures, a decline in mental status, and progressive impairment of consciousness, with a fatal outcome. Despite severely deficient cellular immunity, the elevated antimeasles antibody titers and CSF findings indicated that humoral immunity was not impaired. Histologic, electron microscopic, and immunocytochemical studies revealed the typical intranuclear inclusions of paramyxovirus nucleocapsids, and measles virus antigen in neurons and oligodendrocytes.
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2/26. Measles inclusion-body encephalitis caused by the vaccine strain of measles virus.

    We report a case of measles inclusion-body encephalitis (MIBE) occurring in an apparently healthy 21-month-old boy 8.5 months after measles-mumps-rubella vaccination. He had no prior evidence of immune deficiency and no history of measles exposure or clinical disease. During hospitalization, a primary immunodeficiency characterized by a profoundly depressed CD8 cell count and dysgammaglobulinemia was demonstrated. A brain biopsy revealed histopathologic features consistent with MIBE, and measles antigens were detected by immunohistochemical staining. Electron microscopy revealed inclusions characteristic of paramyxovirus nucleocapsids within neurons, oligodendroglia, and astrocytes. The presence of measles virus in the brain tissue was confirmed by reverse transcription polymerase chain reaction. The nucleotide sequence in the nucleoprotein and fusion gene regions was identical to that of the Moraten and Schwarz vaccine strains; the fusion gene differed from known genotype A wild-type viruses.
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3/26. Uncommon histopathological findings in fatal measles infection: pancreatitis, sialoadenitis and thyroiditis.

    AIMS : We report uncommon histopathological findings in fatal measles infection. methods AND RESULTS : We describe the autopsies of four patients who died during a measles outbreak in Sao Paulo, brazil, in 1997. Two of the patients were children receiving chemotherapy for non-Hodgkin's lymphoma, one was an adult with acquired immunodeficiency syndrome (AIDS) and the fourth was an apparently healthy woman. All patients had their deaths attributed to measles pneumonia. The autopsies revealed extensive giant cell pneumonia and diffuse alveolar damage, severe acute pancreatitis, necrotizing sialoadenitis and thyroiditis due to measles. Measles antigen was detected in lung tissue using a monoclonal anti-measles antibody. CONCLUSIONS: : pancreatitis, thyroiditis and sialoadenitis are not previously reported histopathological findings in measles infection. pancreatitis is a potentially severe complication and should be considered when treating patients with atypical measles.
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4/26. Acute measles gastric infection.

    We describe the case of a 44-year-old man who was referred for gastroscopy because of abdominal pain. During endoscopy, inflammatory changes of the antrum and corpus mucosa were clearly visible, and biopsy samples from the antrum and corpus mucosa were taken. At histology, routine hematoxylin and eosin staining showed characteristics indicative of so-called ex-helicobacter pylori-gastritis that had developed after antibiotic treatment 2 years ago. Additional large, bizarre inclusion bodies and clusters of multinucleated giant cells were located in the surface epithelium and within the lamina propria. These giant cells had an appearance similar to that of Warthin-Finkeldey cells, which can be found during the prodromal phase of measles infection. Anti-measles virus immunochemistry showed a strong positivity for measles virus antigen within the giant cells. Based on these results, the final diagnosis of morbilliform gastritis was made. To our knowledge, no case of measles gastritis has been described in the literature. Our case report confirms the systemic character of measles virus infection and confirms that measles viral replication can involve the gastric mucosa in addition to the conjunctiva, lung, and intestina.
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5/26. measles virus infection in the placenta of monozygotic twins.

    We report a case of monozygotic twins whose mother was infected with measles at 19 weeks' gestation. One of the twins died in utero at 32 weeks' gestation. The placenta of the stillbirth showed massive fibrin deposition, and some residual trophoblasts contained many inclusion bodies positive for measles virus antigen. Fetal organs and cells other than a few splenic lymphocytes showed no evidence of measles virus infection. The placenta of the surviving infant showed focal intervillous fibrin deposits, and only a few syncytiotrophoblasts were positive for measles virus antigen. At present, 7 months after the delivery, the surviving infant has not developed any sign of measles virus infection. Postpartum course of the mother has been uneventful, although high titers of serum anti-measles virus IgM persisted for 6 months after delivery. This case is informative in the following respects: the villous trophoblasts had diagnostic inclusion bodies and ultrastructural evidence of measles virus infection, the degree of viral involvement within the monochorionic placenta was uneven, both of the twins were virtually free from measles virus infection despite the marked involvement of the placenta, and measles virus infection had persisted in the monochorionic placenta for approximately 13 weeks.
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6/26. Activation of human herpesvirus-6 in children with acute measles.

    Virological and serological studies were carried out prospectively to evaluate the possible activation of human herpesvirus-6 (HHV-6) in 50 infants and children with acute measles by isolation of HHV-6 from peripheral blood and by determining neutralizing antibodies to the virus. All but 5 patients (90%) were seropositive to HHV-6 in the acute stage of measles and 18 (40%) had a significant increase in HHV-6 antibody titers thereafter, whereas only 2 of 27 patients who were initially seropositive to Epstein-Barr virus (EBV) viral capsid antigen (VCA) had a significant rise in antibody titers to EBV VCA. Among 18 patients with a significant increase in HHV-6 titers, the virus was isolated from the peripheral blood mononuclear cells of three patients in the early convalescent stage of measles. These results indicate that activation of HHV-6 may occur frequently a few weeks after primary infection with the measles virus.
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7/26. Fetal growth restriction associated with measles virus infection during pregnancy.

    We report on a 28-week infant with growth restriction starting after 23 weeks' gestation because of measles virus (MV) infection of the mother. Histological findings for the placenta revealed extensive fibrin deposition and necrosis of the villi, and MV antigen was demonstrated in the syncytiotrophoblast by immunostaining. The MV-specific IgM level in the infant was negative, but that of the mother was positive. Therefore, we speculate that growth restriction is not attributed to direct infection with MV, but to placental dysfunction due to a decrease in intravillous blood flow and oxygen supply to the fetus.
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8/26. Measles associated with coronary arteritis.

    A two-year-old girl with measles virus (MV) and chronic Epstein-Barr virus (EBV) infection developed lethal coronary aneurysmal arteritis accompanied by giant cell pneumonia, systemic lymphadenitis and hepatosplenomegaly. In her coronary arteries, lungs and aorta, cells containing intranuclear and intracytoplasmic inclusions, including syncytial giant cells, were detected, the presence of MV in the organs being proved by electron microscopic and immunofluorescent studies. Immunopathology further demonstrated MV to be disseminated in almost all organs other than lymph nodes. Clinical diagnosis of chronic EBV infection was established on the basis of persistent high titers of antibodies against capsid and early antigens of EBV and viral presence was confirmed by Southern blot hybridization in a mesenterial lymph node obtained at autopsy. To the best of our knowledge, this is the first description of MV association with coronary aneurysmal arteritis, raising the possibility that measles infection can cause severe vasculitis under immuno-suppressive states, such as that caused by chronic EBV infection.
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9/26. fetal death associated with measles virus infection of the placenta.

    A case of fetal death at 25 weeks' gestation, which was associated with maternal measles infection, is described. Immunohistochemical study revealed measles virus antigen in the syncytial trophoblastic cells and decidua but not in the fetus. Results suggest that fetal death was caused by measles virus infection in the placenta. As far as we know, this is the first report in which a measles virus antigen was detected in the placenta by the immunohistochemical method.
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10/26. Transient disappearance of immunologic disorders and remission after intercurrent measles infections in children with chronic idiopathic thrombocytopenic purpura.

    In two children with chronic idiopathic thrombocytopenic purpura (ITP) a transient remission of thrombocytopenia was observed after intercurrent measles infection. Both cases were girls who had a long history of thrombocytopenia. During acute measles infection, the delayed hypersensitivity response was suppressed. Total T lymphocytes, T-cell subsets, especially OKT4 cells, the lymphoproliferative response, and interleukin-2 (IL-2) and gamma-interferon production were decreased accompanying normalization of the OKT4/OKT8 ratio. However, OKT4 cells remained at a reasonably low level and the lymphoproliferative response stimulated with pokeweed mitogen was still in the lower normal range. Direct immunofluorescent study demonstrated that the measles antigen was present in the mononuclear cells, especially OKT4 cells. The levels of platelet-associated IgG antibody (PAIgG) and IgG circulating immune complex (CIC) were undetectable. One month later, the OKT4/OKT8 ratio lymphoproliferative response significantly increased, IL-2 and gamma-interferon production increased, and PAIgG and IgG CIC reappeared with the relapse of thrombocytopenia. There was also a significant increase in in vitro IgG production due to the presence of patient OKT8 cells and/or OKT4 cells. However, there was no enhancement in the presence of patient B cells. This suggests that the presence of specific OKT4 helper T cells and a defect in the suppressor function of suppressor OKT8 cells contribute to an overproduction of IgG and the appearance of PAIgG accompanied by thrombocytopenia. The transient remission associated with measles infection is probably related to the effect of the virus on the helper T cells, resulting in a decrease in specific OKT4 helper T cells and normalization of the OKT4/OKT8 ratio, suppression of IL-2 and gamma-interferon production, and platelet-associated IgG production.
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