A case of meningoencephalitis associated with G1P[8] rotavirus infection in a Japanese child

Goto, Tamako; Kimura, Hirokazu; Numazaki, Kei; Akiyama, Miho; Katô, Masahiko; Noda, Masahiro; Nozaki, Yasuyuki; Tanaka‐Taya, Keiko; Taniguchi, Kiyosu; Yamagata, Takanori; Nishio, Osamu; Oogane, Teruko; Momoi, Mariko Y.; Okabe, Nobuhiko

doi:10.1080/00365540701466249

Cited by 4 publications

(3 citation statements)

References 18 publications

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“…Typically, rotavirus gastroenteritis begins with a mild‐to‐moderate fever and vomiting, followed by the onset of frequent watery stools. While the clinical complaints are generally intestinal, there is evidence of disease outside the gastrointestinal tract, including elevated liver transaminases, 1 benign infantile convulsions, 2 severe central nervous system disease, 3 and necrotizing enterocolitis (NEC) 4 . In this paper, we report an infant with severe hematemesis and melena, caused by an acute duodenal ulcer associated with rotavirus infection.…”

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confidence: 94%

An infant with rotavirus infection presenting as a severe acute duodenal ulcer

Nejihashi

Sakano

Ono

et al. 2011

Pediatrics International

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Key words acute duodenal ulcer, infant, rotavirus.Rotavirus is an important pathogen causing human viral gastroenteritis during infancy. Typically, rotavirus gastroenteritis begins with a mild-to-moderate fever and vomiting, followed by the onset of frequent watery stools. While the clinical complaints are generally intestinal, there is evidence of disease outside the gastrointestinal tract, including elevated liver transaminases, 1 benign infantile convulsions, 2 severe central nervous system disease, 3 and necrotizing enterocolitis (NEC). 4 In this paper, we report an infant with severe hematemesis and melena, caused by an acute duodenal ulcer associated with rotavirus infection. Case reportA 9-month-old female infant, who was born at 40 weeks' gestation weighing 3,094 g, was referred to us because of severe hematemesis and melena. Initially, she developed vomiting, watery diarrhea, and a temperature of 38.6°C. She was treated with a 7-mg domperidone suppository twice, but no antipyretic. On the third day of her illness, severe hematemesis and melena developed abruptly and she was brought to our hospital by ambulance.On admission, the patient was apathetic and cyanotic, without pyrexia, and failed to respond well to external stimuli. Her skin was pale and dry. Her pulse was 170/min and weak and the blood pressure was 70/0 mmHg. The abdomen was flat and soft. Routine hematological examinations showed a white blood cell count of 15,600/mL, a platelet count of 35.2 ¥ 10 4 /mL, a C-reactive protein less than 0.2 mg/dL, and severe anemia, with hemoglobin of 7.1 g/dL and a hematocrit of 21.1%. The activated partial thromboplastin time, prothrombin time, and hepaplastin test results were 40.5 s, 54.3% (prothrombin time-international normalized ratio 1.42), and 42.0%, respectively. Increased blood urea nitrogen of 22.8 mg/dL and uric acid of 14.7 mg/dL were found, associated with dehydration and a large amount of intestinal bleeding. Blood gas analysis showed metabolic acidosis: pH 7.176, HCO 3 -11.1 mmol/L, and base excess 17.0 mmol/L. The stool was negative for pathogenic bacteria, including Clostridium difficile toxins A and B, and Helicobacter pylori (H.pylori) antigen, but positive for rotavirus. Other viral studies were negative, including cytomegalovirus and Epstein-Barr virus. Ultrasonography of the abdomen revealed a thick gastric wall. Computed tomography to detect a bleeding site showed the thick gastric wall and suggested bleeding at the duodenal cap (Fig. 1). Endoscopy revealed a broad ulcer of the duodenal cap with blood coagula filling the duodenal lumen (Fig. 2a). Biopsy was not carried out because of the risk of re-bleeding.Treatment with a fluid bolus was started immediately, followed by a red blood cell transfusion, and fresh frozen plasma was also given. Intravenous administration of a proton-pump inhibitor and antacid was begun and the patient made favorable progress. Antibodies against H. pylori on admission and 2 months later were negative. Endoscopic examination 2 months later showed disappearan...

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confidence: 94%

An infant with rotavirus infection presenting as a severe acute duodenal ulcer

Nejihashi

Sakano

Ono

et al. 2011

Pediatrics International

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“…[7] Rotavirus infections rarely cause other complication and for a well-managed child, the prognosis is excellent. [8,9] There are reports of complication involving the central nervous system (CNS) where rotavirus was detected in the cerebro-spinal fluid (CSF) in cases of encephalitis and meningitis [10][11][12] and recent studies have confirmed that rotavirus infection is not always confined to gut, but can cause viremia. [13] Hence, this study was undertaken to find out characterization of rotavirus in stool sample which was paired with other sample like serum, urine and saliva in children below 5 years hospitalized for acute diarrhea in order to study the extent of viremia.…”

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confidence: 99%

Characteristics of rotavirus gastroenteritis in hospitalized children in Pune

Borade¹,

Bais²,

Bapat³

et al. 2010

Indian J Med Sci

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It is concluded that in spite of clean hygienic condition and vaccination rotavirus is still an important cause of infantile diarrhea in urban area like Pune. There is association between the occurrence of rotavirus and degree of dehydration, fever, vomiting, and pain in abdomen. Peak incidence was found in the months of December and January. There is association between the occurrence of rotavirus in stool and rotavirus in blood.

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“…The analysis of the literature revealed 794 publications, 83 of which were included in this systematic review (Figure 1). Out of these, 68 permitted a detailed analysis of cases 4–8,11,17–78 while 15 publications, dealing with CwG and rotavirus infection, only reported prevalence and therefore did not allow a detailed analysis 10,48,79–91 . Although these latter 15 publications were not included in the systematic analysis, they were used to calculate the prevalence of CwG in rotavirus infection or the prevalence of rotavirus infection in patients with CwG (Figure 1).…”

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confidence: 99%

Neurological complications of rotavirus infection in children: A systematic review and meta‐analysis

et al. 2023

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Rotavirus is a common cause of benign, self-limiting gastroenteritis in childhood. 1,2 Apart from dehydration and electrolyte imbalance, several neurological complications have been described in rotavirus infections in recent years, such as encephalitis, cerebellitis and a condition described as benign convulsions with mild gastroenteritis (CwG). [3][4][5][6] A direct viral pathomechanism has been postulated since the virus was first detected in the cerebrospinal fluid of a patient suffering from encephalitis in 1995 4 and in subsequent reports. 6,7 CwG was first described in 1982 by Morooka et al. in patients who presented with convulsions associated with mild gastroenteritis without fever or laboratory abnormalities. 3 The definition of CwG was further elaborated in 1992 by Komori et al. as convulsions in

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A case of meningoencephalitis associated with G1P[8] rotavirus infection in a Japanese child

Cited by 4 publications

References 18 publications

An infant with rotavirus infection presenting as a severe acute duodenal ulcer

An infant with rotavirus infection presenting as a severe acute duodenal ulcer

Characteristics of rotavirus gastroenteritis in hospitalized children in Pune

Neurological complications of rotavirus infection in children: A systematic review and meta‐analysis

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