First report of Guillain-Barré syndrome after rotavirus-induced gastroenteritis in a very young infant

Smeets, Carolina C J; Brussel, Wim; Leyten, Q.H.; Brus, F

doi:10.1007/s004310050057

Cited by 9 publications

(6 citation statements)

References 3 publications

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“…Numerous investigators report rotavirus antigen and/or viral RNA detected by enzyme immunoassay, immune electron microscopy, electron microscopy, or reverse transcription-PCR in the central nervous system (CNS) of children with rotavirus diarrhea and with benign to severe convulsions or encephalitis (3, 7-9, 12, 13, 17, 20, 21, 30-32). Additional reports discuss CNS complications with concomitant rotavirus infection but do not demonstrate CNS invasion (11,26,28). Rotavirus antigen and/or RNA was also observed in the microvasculature of the heart (not the myocytes or fibroblasts) of two children who presented with gastroenteritis but suffered cardio-respiratory failure and died (14) and in liver biopsy tissue from infants with cholestatic disease (22,24).…”

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confidence: 99%

A Lymphatic Mechanism of Rotavirus Extraintestinal Spread in the Neonatal Mouse

Mossel

Ramig

2003

J Virol

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We used the neonatal mouse model of rotavirus infection and virus strains SA11-clone 4 (SA11-Cl4) and Rhesus rotavirus (RRV) to examine the mechanism of the extraintestinal spread of viruses following oral inoculation. The spread-competent viruses, RRV and reassortant R7, demonstrated a temporal progression from the intestine, to the terminal ileum, to the mesenteric lymph nodes (MLN), and to the peripheral tissues. SA11-Cl4 was not found outside the intestine. Reassortant virus S7, which was unable to reach the liver in previous studies (E. C. Mossel and R. F. Ramig, J. Virol. 76:6502-6509, 2002), was recovered from 60% of the MLN, suggesting that there are multiple determinants for the spread of virus from the intestine to the MLN. Phenotypic segregation analysis identified RRV genome segment 6 (VP6) as a secondary determinant of the spread of virus to the MLN (P ‫؍‬ 0.02) in reassortant viruses containing segment 7 from the spreadincompetent parent. These data suggest that in the orally infected neonatal mouse, the extraintestinal spread of rotavirus occurs via a lymphatic pathway, and the spread phenotype is primarily determined by NSP3 and can be modified by VP6.

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confidence: 99%

A Lymphatic Mechanism of Rotavirus Extraintestinal Spread in the Neonatal Mouse

Mossel

Ramig

2003

J Virol

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“…In the case reported here, the patient had a history of rotavirus gastroenteritis and upper respiratory tract infection 47 and 14 days, respectively, before admission. Rotavirus, however, had not been described as an antecedent infection in GBS until Smeets et al [7] reported a case of 20-month-old boy who presented with weakness of lower extremities after rotavirus infection. A prospective study has shown that peak incidence of antecedent symptoms of infection is between 1 and 2 weeks prior to GBS onset.…”

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confidence: 96%

“…Although in many clinical situations the responsible organism is not identified, Campylobacter jejuni is the most frequent among a variety of infectious agents associated with GBS. However, there are few reports suggesting the association of rotavirus and GBS [7]. We describe here acute motor-sensory axonal GBS with left facial nerve paralysis in a child with preceding rotavirus infection.…”

Section: Introductionmentioning

confidence: 90%

Acute motor-sensory axonal Guillain–Barré syndrome with unilateral facial nerve paralysis after rotavirus gastroenteritis in a 2-year-old boy

Kamihiro

Higashigawa

Yamamoto

et al. 2012

Journal of Infection and Chemotherapy

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“…The virus may cause afebrile seizures and encephalopathy without any liquid, electrolyte and metabolic problems. Cerebellar involvement, mutism, transient splenial lesions, dancing eyes, acute disseminated encephalomyelitis, Guillain-Barré syndrome have been described with rotavirus gastroenteritis (9,10). Generally, these patients present with disturbance of consciousness or seizures.…”

Section: Discussionmentioning

confidence: 99%

Posterior Reversible Leukoencephalopathy Syndrome with Rotavirus Gastroenteritis

Çelik¹,

Çelik²

2015

J Pediatr Inf

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ÖzetRotavirus çocuklardaki ağır gastroenteritin primer nedenidir. Genellikle rotavirüs enfeksiyonu barsakta lokalizedir ancak barsak dışı tutulumlar raporlanmıştır. Zaman zaman santral sinir sistemi bulgularıyla seyretmektedir. Bu yazıda, 6 aylık erkek çocuktaki rotavirüs ishali sırasında gelişen posterior reversible lökoensefalopati sendromu (PRES) sunulmuştur. AbstractRotavirus is the primary cause of severe gastroenteritis in children. Generally, rotavirus infection is localized in the intestine, but there are some reports with extraintestinal involvement. It is occasionally associated with the central nervous manifestations. Herein, we report posterior reversible leukoencephalopathy syndrome in a 6-month-old boy with rotavirus gastroenteritis. (J Pediatr Inf 2015; 9: 126-9)

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First report of Guillain-Barré syndrome after rotavirus-induced gastroenteritis in a very young infant

Cited by 9 publications

References 3 publications

A Lymphatic Mechanism of Rotavirus Extraintestinal Spread in the Neonatal Mouse

A Lymphatic Mechanism of Rotavirus Extraintestinal Spread in the Neonatal Mouse

Acute motor-sensory axonal Guillain–Barré syndrome with unilateral facial nerve paralysis after rotavirus gastroenteritis in a 2-year-old boy

Posterior Reversible Leukoencephalopathy Syndrome with Rotavirus Gastroenteritis

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