Cases reported "Enterovirus Infections"

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11/78. Congenital enterovirus 71 infection: a case study with virology and immunohistochemistry.

    Previously reported enterovirus 71 (EV71) infections associated with hand-foot-mouth disease, aseptic meningitis, encephalitis, polio-like myelitis, and paralysis all have involved young children. We report a 28-year-old woman who possibly contracted EV71 infection during pregnancy. Obstetric ultrasonograms at 25 weeks of gestation revealed an abnormal placenta, as well as hepatosplenomegaly, liver calcification, excessive ascites, and mild hydrocephalus of the fetus. Presence of EV71 was determined by immunodot blotting, virus culture, and partial sequencing of the amplified product of nested reverse transcription-polymerase chain reaction. Postmortem immunohistochemistry further identified EV71 in the fetal midbrain and liver. The findings indicate that intrauterine EV71 infection is possible during pregnancy. ( info)

12/78. Successful treatment of enterovirus infection with the use of pleconaril in 2 infants with severe combined immunodeficiency.

    Two patients with severe combined immunodeficiency and enterovirus infections were successfully treated with pleconaril. There were no adverse affects. ( info)

13/78. Lympho-monocytic enteroviral myocarditis: traditional, immunohistological and molecularpathological methods for diagnosis in a case of suspected sudden infant death syndrome (SIDS).

    A 7-month-old boy was found lifeless in his bed by his grandfather. Near the mouth there were some blood and chyme on the bedlinen. His mother reported a chill during the last 8 days. autopsy revealed multiple petechia under the capsule of the thymus, subepicardially and subpleurally, the cause of death was tentative supposed to be a sudden infant death. Histologically parts of the myocardium showed a lympho-monocytic myocarditis according to the DALLAS-criteria. Immunohistological investigations demonstrated an enhanced expression of MHC class II antigens, an increased number of leucocytes as well as t-lymphocytes. in situ hybridization and immunohistochemistry revealed myocardial enterovirus infection. Considering that there were regions in the myocardium without the traditional findings of myocardial necrosis and inflammation but with distinct expression of the above mentioned immunohistologic markers, immunohistological investigations turn out to be an appropriate tool to examine infant fatalities with uncertain cause of death for early stages of myocarditis. ( info)

14/78. First fatal case of enterovirus 71 infection in hong kong.

    Enteroviruses are a common cause of childhood infections, from hand, foot and mouth disease, to lethal brainstem encephalitis. Enterovirus 71 was first isolated in 1969. Brainstem encephalomyelitis and pulmonary oedema are postulated to be causally related and have been found to be a common feature of fatal enterovirus 71 cases. A fatal case of enterovirus 71 infection in a 2-year-old, previously healthy boy is reported. He presented to the Department of Paediatrics with clinical features of sepsis within 3 days of onset of fever. A few minutes after injection of midazolam, fentanyl and vecuronium for intubation, cardiac arrest developed and was not amenable to various treatment modalities. Pulmonary haemorrhage and oedema were noted during intubation, and postmortem examination confirmed the presence of brainstem encephalomyelitis. ( info)

15/78. Echovirus 7 associated encephalomyelitis.

    BACKGROUND: Hand, foot, and mouth disease (HFMD) is endemic in malaysia. In 1997, a large outbreak of enterovirus 71 (EV-71) associated HFMD resulted in 41 deaths due to severe left ventricular dysfunction and central nervous system infection with extensive damage to the medulla and pons. The clinical presentation in all these patients were rapid cardio-respiratory decompensation leading to cardiac arrest. Another large outbreak of HFMD with 55 fatal cases and a similar clinical picture was reported in taiwan in 1998. In 2000, an outbreak of HFMD resulted in the deaths of three children who had rapid cardio-respiratory decompensation and one child who survived a central nervous system infection. OBJECTIVES: We set out to study the etiologic agent and mechanism involved in three children who presented to our hospital, two of whom died and one survived a central nervous system infection. STUDY DESIGN: The clinical course of the disease was described. Throat, rectal swab and cerebrospinal fluid samples were subjected to viral isolation and viral isolates were identified by immunofluorescence, micro-neutralisation using human rhabdomyosarcoma (RD) cells, and reverse transcritpase polymerase chain reaction. magnetic resonance imaging was performed on two of the patients. RESULTS: Echovirus 7 was the sole pathogen isolated from three cases of acute encephalomyelitis, two of which were fatal due to severe left ventricular dysfunction resistant to inotropic support. The survivor had residual bulbar palsy, but is considered to have had a good neurological outcome. CONCLUSION: Echovirus 7 infection associated with encephalomyelitis could be fatal due to indirect involvement of the heart resulting in severe left ventricular dysfunction. In addition one of the children presented with hand, foot, and mouth disease, a syndrome that has not been previously associated with echovirus 7 infection. ( info)

16/78. Echovirus hepatic failure in infancy: report of four cases with speculation on the pathogenesis.

    Disseminated echovirus infection with fulminant hepatic failure occurs almost exclusively in newborns. Although a relatively uncommon condition, it is on occasion associated with neonatal death accompanied by diffuse and extensive hemorrhagic necrosis of the liver and adrenals as the defining finding. We report four cases of severe systemic neonatal echovirus infection and present histologic and clinical evidence to demonstrate the two histologic patterns of liver involvement; intravascular coagulation in the early clinical course and a veno-occlusive component in later stages of the disease. Viral damage to vascular endothelium and hepatic venous endothelium by a "hit-and-run" process in the early viremic phase rather than direct hepatocyte injury is postulated to be a mechanism. ( info)

17/78. Left ventricular dysfunction in children with fulminant enterovirus 71 infection: an evaluation of the clinical course.

    We describe 2 children with typical hand, foot, and mouth disease due to enterovirus 71 infection, 1 of whom died. Both cases were complicated by acute fulminant shock syndrome; the patients had remarkable acute left ventricular dysfunction. The clinical experience indicates that the rapid death associated with fulminant enterovirus rhombencephalitis is the result of rapid cardiogenic shock rather than neurogenic pulmonary edema. ( info)

18/78. Non-progressive viral myelitis in X-linked agammaglobulinemia.

    We report a 14-year-old boy with X-linked agammaglobulinemia (XLA) complicated by isolated non-progressive myelitis caused by Coxsackie virus B1. Despite the absence of immunoglobulin supplement and persistence of the virus for the initial 2 years, motor impairment did not show any progression for 3 years. This report shows that the prognosis of central nervous system infection in XLA is not determined by immunoglobulin levels alone, and that it is not always progressive or fatal. The balance between host immunity and the virulence of the causative virus may be involved in the prognosis of meningoencephalitis in XLA. ( info)

19/78. Generalized myopathy and cerebral malformations possibly related to an enteroviral infection.

    A study was made on a case of generalized muscular hypotonus manifested at birth. Serological findings and epidemiological data suggested an association to a recently described enterovirus infection (enterovirus candidate 71) known to cause neurological disease in man. autopsy revealed cerebral malformations and generalized myopathy compatible with a viral etiology of the disease. ( info)

20/78. Unilateral facial paralysis occurring in an infant with enteroviral otitis media and aseptic meningitis.

    We report the case of a four month old infant presenting to the Emergency Department (ED) with irritability and facial asymmetry following a recent bout of gastroenteritis. physical examination revealed a unilateral peripheral facial nerve paralysis. Common in older children and adults, facial nerve palsy has rarely been described in infancy. Although historically associated with a variety of inflammatory and infectious causes, the pathogenesis remains unclear. In this infant we were able to successfully identify an underlying acute enteroviral infection. Coxsackie B5 was isolated from the middle ear fluid, cerebrospinal fluid (CSF), nasopharyngeal and rectal swabs. After myringotomy drainage of the middle ear fluid and placement of pneumatic equalization tubes, there was rapid and complete resolution of facial paralysis. ( info)
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