Detection of rotavirus in cerebrospinal fluid and blood of patients with convulsions and gastroenteritis by means of the reverse transcription polymerase chain reaction

Nishimura, Shigeyuki; Ushijima, Hiroshi; Nishimura, Shigeo; Shiraishi, Hiroaki; Kanazawa, Chikako; Abe, Toshiaki; Kaneko, Kenitiro; Fukuyama, Yukio

doi:10.1016/0387-7604(93)90088-p

Cited by 112 publications

(65 citation statements)

References 10 publications

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“…This seizure disorder is now considered to represent a situation-related seizure due to rotavirus infection. Rotavirus genomic ribonucleic acid has been detected in CSF from patients with benign convulsions and mild gastroenteritis (17). Severe dehydration and electrolytes imbalance resulting from diarrhea may induce convulsions.…”

Section: Discussionmentioning

confidence: 99%

Acute Symptomatic Seizure Disorders in Young Children—A Population Study in Southern Taiwan

1998

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Summary: Purpose: To determine the incidence, etiology, and prognosis of acute symptomatic seizures in children by age 3 years.Methods: In a population-based birth cohort study of all 15,209 neonatal survivors born in Tainan City between October 1989 and December 1991, parents or caretakers of 13,493 children aged 3 years were surveyed by telephone regarding any provoked convulsive disorder, particularly acute symptomatic seizure, in the children; medical records were reviewed.Results: Sixty-three children (39 boys, 24 girls) had acute symptomatic seizures (incidence 0.46 in 100). The leading causes of acute symptomatic seizures were acute gastroenteritis, encephalitis/encephalopathy, and bacterial meningitis. Agespecific incidence was highest in the group aged 1-12 months. Intracranial hemorrhage, bacterial meningitis, and metabolic disturbance were the major causes of acute symptomatic seizures in children aged 1-12 months. Acute gastroenteritis, encephalitis/encephalopathy, and bacterial meningitis accounted for 85% of the causes in children aged 13-24 months, and gastroenteritis and encephalitislencephalopathy were the predominant causes in those aged 25-36 months. By age 5 years, subsequent unprovoked seizures developed in 14% of the survivors of acute symptomatic seizures.Conclusions: Many acute symptomatic seizures are preventable. The risk of subsequent unprovoked seizures is determined by underlying precipitating factors. Public education regarding the danger of shaken-baby syndrome and excessive water supplement, as well as and nationwide vaccination against bacterial meningitis in young children, is necessary. Key Words: Acute symptomatic seizure-Children.Convulsive disorders represent one of the most common neurological problems in children. Most occur before age 3 years because the causes (fever, metabolic disturbance, head trauma, CNS infection and acute encephalopathy) occur predominantly in early childhood (1,2), Reports indicated that the incidence of epilepsy and unprovoked seizures was focused in industrialized countries (1)(2)(3)(4)(5). In most epidemiological studies, acute symptomatic seizure disorders are usually studied in association with epilepsy, and few such studies have focused on children (3,6,7). In the present study, the incidences, etiology, and prognosis of acute symptomatic seizures in children at age 3 years were investigated in a geographically defined area of southern Taiwan.

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Section: Discussionmentioning

confidence: 99%

Acute Symptomatic Seizure Disorders in Young Children—A Population Study in Southern Taiwan

1998

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“…Rotavirus has been detected in cerebral spinal fluid (35,45,58,61,85), liver and kidney (28), extraintestinal lymphoid tissue (12), and the sera of infected children and animals (9,81). By in situ reverse transcription-PCR, rotavirus was also found in the heart, where it was mainly localized to endothelial cells (53).…”

Section: Discussionmentioning

confidence: 99%

Rotavirus Enterotoxin NSP4 Binds to the Extracellular Matrix Proteins Laminin-β3 and Fibronectin

Boshuizen

Rossen

Sitaram

et al. 2004

J Virol

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“…Although it occurs rarely in immunocompetent children, a growing body of evidence suggests that group A rotavirus infection may spread beyond the intestine with generally unknown clinical consequences. In children, viral antigen and viral RNA have been observed in the central nervous system, liver, and kidney (14,23). Several cases of afebrile seizures with concomitant rotavirus infection have been described (9,18), and one report associated group C rotavirus infection with biliary atresia in humans (34).…”

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confidence: 99%

Rotavirus Genome Segment 7 (NSP3) Is a Determinant of Extraintestinal Spread in the Neonatal Mouse

Mossel

Ramig

2002

J Virol

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We used the neonatal mouse model of rotavirus infection to study extraintestinal spread following oral inoculation. Five-day-old pups were inoculated with either SA11-Cl3, SA11-Cl4, SA11-4F, RRV, or B223. By using virus detection in the liver as a proxy determination for extraintestinal spread, rotavirus strains capable of extraintestinal spread at high frequency (rhesus rotavirus [RRV]) and very low frequency (SA11-Cl4) were identified. Both strains productively infected the gastrointestinal tract. Oral inoculation of mice with RRV/ SA11-Cl4 reassortants and determination of virus titers in the gut and liver revealed that the extraintestinal spread phenotype segregated with RRV genome segment 7 to a high level of significance (P ‫؍‬ 10 ؊3 ). RRV segment 7 also segregated with the growth of virus in the gut (P ‫؍‬ 10 ؊5 ). Although infection of the gut was clearly required for tropism to the liver, there was no correlation between virus titers in the gut and detection of virus in the liver. Five days after intraperitoneal administration to bypass the gut barrier to virus spread, RRV and SA11-Cl4 both were recovered in the liver. However, only RRV was found in the liver following subcutaneous inoculation, suggesting that this peripheral site presented a similar barrier to virus spread as the gut. Sequence analysis of segment 7 from parental RRV and SA11-Cl4 and selected reassortants showed that (i) amino acid differences were distributed throughout the coding sequences and not concentrated in any particular functional motif and (ii) parental sequence was preserved in reassortants. These data support the hypothesis that NSP3, coded for by genome segment 7, plays a significant role in viral growth in the gut and spread to peripheral sites. The mechanism of NSP3-mediated tropism is under investigation.

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Detection of rotavirus in cerebrospinal fluid and blood of patients with convulsions and gastroenteritis by means of the reverse transcription polymerase chain reaction

Cited by 112 publications

References 10 publications

Acute Symptomatic Seizure Disorders in Young Children—A Population Study in Southern Taiwan

Acute Symptomatic Seizure Disorders in Young Children—A Population Study in Southern Taiwan

Rotavirus Enterotoxin NSP4 Binds to the Extracellular Matrix Proteins Laminin-β3 and Fibronectin

Rotavirus Genome Segment 7 (NSP3) Is a Determinant of Extraintestinal Spread in the Neonatal Mouse

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