Suspected rotavirus encephalitis.

Ushijima, Hiroshi; K, Bosu; Abe, Toshiaki; Shinozaki, Tatsuhiko

doi:10.1136/adc.61.7.692

Cited by 69 publications

(40 citation statements)

References 4 publications

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“…Among the etiological agents of acute infectious diarrhea rotaviruses account for nearly 25% of hospital admissions with vomiting and diarrhea followed by severe dehydration in very young children below 2 years of age (Broor et al, 1985). Moreover it has been occasionally associated with encephalopathy, indicating the possible involvement of the central nervous system (CNS) (Ushiyama et al, 1986). However these pathophysiological correlations are still unclear.…”

Section: Introductionmentioning

confidence: 99%

Serum and cerebrospinal fluid nitrite/nitrate levels in patients with rotavirus gastroenteritis induced convulsion

et al. 2004

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Section: Introductionmentioning

confidence: 99%

Serum and cerebrospinal fluid nitrite/nitrate levels in patients with rotavirus gastroenteritis induced convulsion

et al. 2004

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“…In a few cases rotavirus RNA has been detected in cerebrospinal fluid (CSF) 59--61 , possibly associated with meningitis 62 , encephalopathy 63,64 and encephalitis 65,66 .…”

Section: General Pathophysiologymentioning

confidence: 99%

Rotavirus Disease Mechanisms Diarrhea, Vomiting and Inflammation : How and Why

Hagbom¹

2015

Linköping University Medical Dissertations

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Rotavirus infections cause diarrhea and vomiting that can lead to severe dehydration. Despite extensive tissue damage and cell death, the inflammatory response is very limited. The focus of this thesis was to study pathophysiological mechanisms behind diarrhea and vomiting during rotavirus infection and also to investigate the mechanism behind the limited inflammatory response. An important discovery in this thesis was that rotavirus infection and the rotavirus toxin NSP4 stimulate release of the neurotransmitter serotonin from intestinal sensory enterochromaffin cells, in vitro and ex vivo. Interestingly, serotonin is known to be a mediator of both diarrhea and vomiting. Moreover, mice pups infected with rotavirus responded with central nervous system (CNS) activation in brain structures associated with vomiting, thus indicating a cross-talk between the gut and brain in rotavirus disease. Our finding that rotavirus infection activates the CNS led us to address the hypothesis that rotavirus infection not only activates the vagus nerve to stimulate vomiting, but also suppresses the inflammatory response via the cholinergic anti-inflammatory pathway, both of which are mediated by activated vagal afferent nerve signals into the brain stem. We found that mice lacking an intact vagus nerve, and mice lacking the α7 nicotine acetylcholine receptor (nAChR), being involved in cytokine suppression from macrophages, responded with a higher inflammatory response. Moreover, stimulated cytokine release from macrophages, by the rotavirus toxin NSP4, could be attenuated by nicotine, an agonist of the α7 nAChR. Thus, it seems most reasonable that the cholinergic anti-inflammatory pathway contributes to the limited inflammatory response during rotavirus infection. Moreover, rotavirus-infected mice displayed increased intestinal motility at the onset of diarrhea, which was not associated with increased intestinal permeability. The increased motility and diarrhea in infant mice could be attenuated by drugs acting on the enteric nervous system, indicating the importance and contribution of nerves in the rotavirus mediated disease. In conclusion, this thesis provides further insight into the pathophysiology of diarrhea and describe for the first time how rotavirus and host cross-talk to induce the vomiting reflex and limit inflammation. Results from these studies strongly support our hypothesis that serotonin and activation of the enteric nervous system and CNS contributes to diarrhea, vomiting and suppression of the inflammatory response in rotavirus disease

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“…Wong et al (397) reported a case of aseptic meningitis associated with rotavirus gastroenteritis in which rotavirus particles were seen in the cerebral spinal fluid by IEM. Ushijima et al (373) reported on a case of encephalitis that developed during rotavirus gastroenteritis, in which rotavirus immunoglobulin G (IgG) increased in the patient's cerebrospinal fluid. In addition, rotavirus-like particles have been detected by EM and EIA in a liver biopsy in a case of hepatic abscess (139).…”

Section: Epidemiologymentioning

confidence: 99%

Human viral gastroenteritis

Christensen

1989

Clin Microbiol Rev

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During the last 15 years, several different groups of fastidious viruses that are responsible for a large proportion of acute viral gastroenteritis cases have been discovered by the electron microscopic examination of stool specimens. This disease is one of the most prevalent and serious clinical syndromes seen around the world, especially in children. Rotaviruses, in the family Reoviridae, and fastidious fecal adenoviruses account for much of the viral gastroenteritis in infants and young children, whereas the small caliciviruses and unclassified astroviruses, and possibly enteric coronaviruses, are responsible for significantly fewer cases overall. In addition to electron microscopy, enzyme immunoassays and other rapid antigen detection systems have been developed to detect rotaviruses and fastidious fecal adenoviruses in the stool specimens of both nonhospitalized patients and those hospitalized for dehydration and electrolyte imbalance. Experimental rotavirus vaccines have also been developed, due to the prevalence and seriousness of rotavirus infection. The small, unclassified Norwalk virus and morphologically similar viruses are responsible for large and small outbreaks of acute gastroenteritis in older children, adolescents, and adults. Hospitalization of older patients infected with these viruses is usually not required, and their laboratory diagnoses have been limited primarily to research laboratories.

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Suspected rotavirus encephalitis.

Cited by 69 publications

References 4 publications

Serum and cerebrospinal fluid nitrite/nitrate levels in patients with rotavirus gastroenteritis induced convulsion

Serum and cerebrospinal fluid nitrite/nitrate levels in patients with rotavirus gastroenteritis induced convulsion

Rotavirus Disease Mechanisms Diarrhea, Vomiting and Inflammation : How and Why

Human viral gastroenteritis

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