Acute encephalopathy of Bacillus cereus mimicking Reye syndrome

作者：Ichikawa Kazushi^*; Gakumazawa Masayasu; Inaba Aya; Shiga Kentaro; Takeshita Saoko; Mori Masaaki; Kikuchi Nobuyuki

来源：Brain & Development, 2010, 32(8): 688-690.

DOI：10.1016/j.braindev.2009.09.004

• Bacillus cereus
• Cereulide
• Encephalopathy
• Reye syndrome
• Beta-oxidation
• Hypothermia
• High-dose methylprednisolone

We present an 11-year-old boy diagnosed as having acute encephalopathy and liver failure with the underlying condition of a metabolic dysfunction. He developed convulsions and severe consciousness disturbance following gastroenteritis after the ingestion of some fried rice. He showed excessive elevation of transaminases, non-ketotic hypoglycemia and hyperammonemia, which were presumed to reflect a metabolic dysfunction of the mitochondrial beta-oxidation, and he exhibited severe brain edema throughout the 5th hospital day. He was subjected to mild hypothermia therapy for encephalopathy, and treated with high-dose methylprednisolone, cyclosporine and continuous hemodiafiltration for liver failure, systemic organ damage and hyperammonemia. The patient recovered with the sequela of just mild intelligence impairment. In this case, Bacillus cereus, producing emetic toxin cereulide, was detected in a gastric fluid specimen, a stool specimen and the fried rice. It was suggested that the cereulide had toxicity to mitochondria and induced a dysfunction of the beta-oxidation process. The patient was considered as having an acute encephalopathy mimicking Reye syndrome due to food poisoning caused by cereulide produced by B. cereus.

• 出版日期2010-9