Cases reported "Echovirus Infections"

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1/5. Acute onset of type I diabetes mellitus after severe echovirus 9 infection: putative pathogenic pathways.

    enterovirus infections have been implicated in the development of type I diabetes mellitus. They may cause beta cell destruction either by cytolytic infection in the pancreas or indirectly by contributing to autoimmune reactivity. We sought evidence for these 2 mechanisms in a case of acute-onset diabetes mellitus that occurred during severe echovirus 9 infection. The virus was isolated and administered to cultured human beta cells. No viral proliferation was observed, and no beta cell death was induced, while parallel exposure to Coxsackie B virus serotype 3 resulted in viral proliferation and massive beta cell death. Although the viral protein 2C exhibited a sequence similar to that of the beta cell autoantigen glutamic acid decarboxylase (GAD(65)), no cross-reactive T cell responses were detected. The patient did not develop antibodies to GAD(65) either. Absence of evidence for direct cytolytic action or an indirect effect through molecular mimicry with GAD(65) in the present case raises the possibility of another indirect pathway through which enteroviruses can cause diabetes mellitus.
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2/5. Fatal neonatal echovirus 6 infection: autopsy case report and review of the literature.

    A full-term, healthy male neonate was delivered by caesarian section to a 26-year-old primigravida woman who had a history of fever and upper respiratory tract infection. On the fourth day of life, the neonate developed a sepsis-like syndrome, acute respiratory and renal failure, and disseminated intravascular coagulopathy. He died 13 days after birth. Postmortem examination revealed jaundice, anasarca, massive hepatic necrosis, adrenal hemorrhagic necrosis, renal medullary hemorrhage, hemorrhagic noninflammatory pneumonia, and severe encephalomalacia. Echovirus type 6 was isolated from blood, liver, and lungs. Although uncommon, echovirus type 6 infection may produce a spectrum of pathologic findings similar to those seen with the more commonly virulent echovirus type 11.
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3/5. Severe neonatal enteroviral hepatitis treated with pleconaril.

    Neonatal enteroviral hepatitis carries high morbidity and mortality. We treated three full term neonates with severe enteroviral hepatitis with pleconaril on an open label compassionate use protocol. Each mother had history of a viral-like syndrome within 1 week before delivery. The neonates presented at 4 to 5 days of age with fulminant hepatic failure with severe coagulopathy, and each yielded an echovirus. All were treated with pleconaril (VP63843) at 5 mg/kg every 8 h by nasogastric tube. Two of the three neonates with life-threatening enteroviral hepatitis recovered fully. Further experience with pleconaril for neonatal enteroviral hepatitis is warranted.
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4/5. Echovirus 11 infections of newborns with mortality during the 1979 enterovirus season in Milwaukee, Wis.

    Echovirus serotype 11 (ECHO-11) was implicated in three neonatal deaths during an enterovirus outbreak from July through October 1979 in Milwaukee. The deaths followed congenital infections acquired in the community during late pregnancy. Two of the three ECHO-11 and one Coxsackie B4 deaths of infants occurred after cesarean section deliveries. Of 225 confirmed echovirus infections, 30 to 45 percent occurred in infants under 60 days old, 54 to 67 percent in the first year of life, and 13 to 25 percent in the over-10 age groups. In 13 cases with onset of symptoms in the first week of life. 8 (including the 4 fatalities) were acquired congenitally; 6 of the 8 were associated with ECHO-11, 2 with ECHO-7, and 1 with Coxsackie B4. ECHO-7 and 30 other predominant strains were isolated during the outbreak, but none was associated with mortality or severe disease in neonates. At a Milwaukee hospital, a temporal association was observed between echovirus infection, particularly ECHO-11, and increased numbers of stillbirths.
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5/5. 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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