Cases reported "Echovirus Infections"

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1/7. Neonatal Type I diabetes associated with maternal echovirus 6 infection: a case report.

    AIMS/HYPOTHESIS: Neonatal diabetes mellitus is rare, and it has not been associated with beta-cell autoimmunity. Enteroviral infections during pregnancy have been implicated as a risk factor for the later development of Type I (insulin-dependent) diabetes mellitus. We now report of a baby girl who was born severely growth-retarded with neonatal insulin-deficient diabetes, and look for evidence of intrauterine enteroviral infections and beta-cell targeted autoimmunity. methods: Diabetes-associated autoimmunity was studied by measurement of several types of islet cell reactive autoantibodies. The infant's T-cell responses to insulin and enterovirus antigens were recorded and enterovirus antibodies were measured both from the mother and the child. RESULTS: Several types of diabetes-associated autoantibodies were detected postnatally, including insulin autoantibodies, conventional islet cell autoantibodies and glutamic acid decarboxylase antibodies, whereas no autoantibodies were observed in the mother. The infant's T-cells showed reactivity to insulin and purified enterovirus particles. Based on serological studies, the pathogenetic process could have been triggered by an echovirus 6 infection during pregnancy. The patient's diabetes has been permanent, although there were signs of endogenous insulin production for several months. exocrine pancreatic insufficiency was diagnosed at the age of 1 year. CONCLUSION/INTERPRETATION: These observations suggests that enteroviral infections may induce beta-cell autoimmunity even in utero.
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2/7. Severe echovirus 30 infection in twin neonates.

    Although enteroviruses can cause overwhelming and fatal systemic infections in neonates, such severe neonatal infections remain uncommon and rarely involve both of twin neonates at the same time. We report the cases of twin neonates who developed fever initially, and then progressed to disseminated systemic disease with marked thrombocytopenia, coagulopathy, and hepatic failure. One of the neonates died and the other survived. Both neonates were treated with intravenous immunoglobulin and maternal fresh frozen plasma was also given to the neonate who survived. Virus cultures from the nasopharynx, rectum and cerebral spinal fluid of both neonates yielded enterovirus, later typed as echovirus 30. The surviving neonate had normal development without obvious sequelae during a follow-up period of 1 year. The major determinant of the survival from severe neonatal enterovirus infection might have been the pre-existing severity of the disease before treatment, and complete recovery could be expected if the infant survived the acute stage of illness.
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3/7. Echovirus 11 sepsis in a neonate: report of one case.

    Neonates infected with nonpolio enteroviruses are at high risk for developing significant illness, including sepsis-like illness, meningoencephalitis, myocarditis and/or hepatitis. Echoviruses and group B coxsackieviruses account for the majority of neonatal enterovirus infections. We reported a case of echovirus 11 infection in newborn associated with maternal infection. To our knowledge, this is the first reported fatal case of neonatal echovirus infection in taiwan. Eventually, the baby expired because of severe sepsis-like illness, fulminant hepatitis, disseminated intravascular coagulation, and extensive hemorrhagic manifestations in spite of intensive care, intravenous immunoglobulin infusion and exchange transfusion.
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4/7. Congenital echo virus infection--morphological and virological study of fetal and placental tissue.

    A prospective study of 78 pregnant women was undertaken to detect maternal enterovirus infection. Maternal faecal specimens and blood samples, placental and fetal tissue were taken for viral study, electron microscopy, histochemistry, and morphological examination. We present the post-mortem findings in three fetuses whose maternal infection was detected before delivery by isolation of ECHO virus type 33 and type 27 from faecal specimens and/or placental and fetal tissues. The morphological aspects were similar in all cases and included an acute infection of the placenta and hypoxic/hypotensive injury to fetal organs. In one case, viral particles were detected by electron microscopy of the fetal liver. This series of cases of intrauterine ECHO virus infection confirms the potential gravity of such infection during pregnancy and the need to prevent enteroviral disease.
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5/7. Disseminated neonatal echovirus 11 disease following antenatal maternal infection with a virus-positive cervix and virus-negative gastrointestinal tract.

    An infant girl was born apparently well one week after her mother had had a mild illness with chills, fever, and diarrhea. On the third day of life, the infant became ill and died four days later with necrotizing hepatitis. On the same day, echovirus type 11 was recovered from the throat, rectum, and buffy coat of the infant and from the cervix of the mother. At this time, the mother had an IgM neutralizing antibody titer to echovirus type 11 and 1:128, but no IgG antibodies. The infant had no echovirus type 11 antibodies. The virus was also isolated from the baby's liver and adrenal at autopsy. These findings raise the possibility of enterovirus infection at delivery from a contaminated cervix.
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6/7. Fatal echovirus 11 disease in premature neonates.

    Four cases of fatal echovirus 11 disease occurred in premature infants during a community outbreak of enteroviral disease in massachusetts in 1979. Each infant developed nonspecific symptoms and jaundice at 4 to 6 days of age, and subsequent progressive hepatic failure and generalized bleeding. Only one infant survived longer than six days. Virus was recovered from multiple sites premortem, and from virtually all tissue cultured at autopsy. myocarditis was not present clinically or pathologically. Clinical and laboratory evidence implicated perinatal transmission of virus from mother to infant. Three mothers experienced a febrile illness with abdominal pain within the last five days of pregnancy. In two, the illness led to a false diagnosis of abruptio placenta and interruption of pregnancy by cesarian section. review of case reports of this syndrome caused by other echovirus serotypes revealed that many had similar perinatal events. Each mother ultimately developed neutralizing antibody to echovirus 11. However, all four infants were born without passively acquired antibody, probably because they were delivered prior to the appearance of specific maternal IgG. Although laboratory studies by others have shown other factors may be responsible for the ability of enterovirus to cause overwhelming disease in neonates, uncontrolled data from these four infants and their mothers suggest that timing of maternal illness in relation to delivery of the infant may also be important.
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7/7. Fatal ECHO 24 infection in a patient with hypogammaglobulinemia: relationship to dermatomyositis-like syndrome.

    patients with deficient antibody-mediated immunity may develop a rare "dermatomyositis-like" syndrome, which is usually progressive and fatal. We have observed a child with hypogammaglobulinemia in whom a dermatomyositis-like syndrome was associated with a fatal, disseminated ECHO 24 infection. This association suggests that in some immunodeficient patients the fatal dermatomyositis-like syndrome is a manifestation of a viral infection in a compromised host. The use of maternal plasma, with a high titer of ECHO 24 neutralizing activity, was unsuccessful in arresting the progress of the infection.
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