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Intestinal pseudo-obstruction and acute pandysautonomia associated with Epstein-Barr virus infection
M Besnard1, C Faure, G Fromont-Hankard
1Department of Pediatric Gastroenterology, Hôpital Robert Debré, Paris, France.
Insights
Epstein-Barr virus (EBV) reactivation caused neurological and intestinal issues in a child, leading to acquired hypoganglionosis. This case highlights EBV
Area of Science:
- Virology
- Pediatric Neurology
- Gastroenterology
Background:
- Epstein-Barr virus (EBV) is a common human herpesvirus.
- EBV reactivation is typically associated with infectious mononucleosis, but can have varied clinical manifestations.
- Neurological and gastrointestinal complications are rare sequelae of EBV infection.
Observation:
- A previously healthy 13-year-old boy presented with pharyngitis and acute abdominal ileus.
- Postoperatively, the patient developed prolonged intestinal obstruction, pandysautonomia, and encephalomyelitis.
- Histological examination revealed hypoganglionosis in the rectum and appendix, with inflammatory infiltrates near neural plexuses.
Findings:
- Epstein-Barr virus (EBV) was detected in blood, cerebrospinal fluid, appendix, mesenteric lymph node, and gastric biopsies.
- In situ hybridization confirmed EBV presence in the myenteric neural plexuses.
- The patient exhibited EBV spontaneous lymphocytic proliferation and serological evidence of recent/reactivated infection.
Implications:
- This case suggests Epstein-Barr virus (EBV) reactivation can be a direct cause of acquired hypoganglionosis and neurointestinal disorders.
- The findings underscore the potential for EBV to induce significant neurological and gastrointestinal pathology in previously healthy individuals.
- This report is the first to document acquired hypoganglionosis attributed to EBV reactivation.
Abstract:
We report the association of neurological and intestinal disorders with the reactivation of Epstein-Barr virus (EBV) in a child. This previously healthy 13-yr-old boy presented with pharyngitis and acute abdominal ileus. Laparotomy excluded a mechanical obstruction. Postoperatively, he suffered from prolonged intestinal obstruction, pandysautonomia, and encephalomyelitis. Histological examination of the appendix and a rectal biopsy taken 3 months after the onset showed an absence of ganglion cells (appendix) and hypoganglionosis (rectum), with a mononucleate inflammatory infiltrate in close contact with the myenteric neural plexuses. EBV-PCR was positive in the blood and cerebrospinal fluid, and in situ hybridization with the Epstein-Barr virus encoded RNA probe showed positive cells throughout the appendix wall including the myenteric area, in a mesenteric lymph node, and in the gastric biopsies. EBV spontaneous lymphocytic proliferation was noted in the blood. The serology for EBV showed previous infection but anti-early antigen antibodies were present. No immunodeficiency was found. Neurological and GI recovery occurred after 6 months of parenteral nutrition and bethanechol. The omnipresence of EBV associated with the neurointestinal symptoms suggest that the virus was the causal agent. This is the first documented case of acquired hypoganglionnosis due to EBV reactivation.