Fulminant liver failure in association with the emetic toxin of Bacillus cereus

Fulminant liver failure in association with the emetic toxin of Bacillus cereus
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DOI:
10.1056/nejm199704173361604
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发表时间:
1997-04-17
影响因子:
158.5
通讯作者:
Krahenbuhl, S
Krahenbuhl, S
中科院分区:
医学1区
文献类型:
--
作者:
Mahler, H;Pasi, A;Krahenbuhl, S

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一名17岁的男孩和他的父亲在吃了四天前准备的意大利面和香蒜沙司后患上了急性胃肠炎。两天之内,男孩出现暴发性肝功能衰竭和横纹肌溶解,死亡。父亲患有高胆红素血症和横纹肌溶解症,但已康复。我们调查了这些疾病的起因。方法采用常规方法对细菌进行分离鉴定,采用免疫测定法和细胞培养法对细菌毒素进行定量测定。分析了分离的毒素对大鼠肝脏线粒体中各种底物氧化速率的影响。结果男孩的肝脏尸检显示弥漫性微泡性脂肪变性和中带状坏死,表明由于线粒体毒素导致肝脏线粒体β -氧化受损。没有证据表明摄入了重金属、卤化化合物、肝毒性药物或葡萄球菌肠毒素。然而,在用于重新加热食物的锅的残留物以及男孩的肝脏和胆汁中都发现了高浓度的蜡样芽孢杆菌催吐毒素。从肠道内容物和锅渣中培养蜡样芽孢杆菌。从蜡样芽孢杆菌培养物中分离出的催吐毒素是一种线粒体毒素。结论该患者在摄入受蜡样芽孢杆菌毒素污染的食物后发生暴发性肝衰竭,该毒素抑制肝脏线粒体脂肪酸氧化,提示其导致了该患者的肝衰竭。(C) 1997年,马萨诸塞州医学协会。
Background A 17-year-old boy and his father had acute gastroenteritis after eating spaghetti and pesto that had been prepared four days earlier. Within two days, fulminant liver failure and rhabdomyolysis developed in the boy and he died. The father had hyperbilirubinemia and rhabdomyolysis but recovered. We investigated the cause of these illnesses.Methods Bacteria were isolated and characterized by conventional methods, and bacterial toxins were quantified by immunoassays and cell-culture techniques. The effect of the isolated toxin on the rates of oxidation of various substrates was analyzed in rat-liver mitochondria.Results Autopsy of the boy's liver revealed diffuse microvesicular steatosis and midzonal necrosis that suggested impaired beta-oxidation of liver mitochondria due to a mitochondrial toxin. There was no evidence of ingestion of heavy metals, halogenated compounds, hepatotoxic drugs, or staphylococcal enterotoxin. However, high concentrations of Bacillus cereus emetic toxin were found both in the residue from the pan used to reheat the food and in the boy's liver and bile. B. cereus was cultured from the intestinal contents and the pan residue. The emetic toxin isolated from the B. cereus cultures was found to be a mitochondrial toxin.Conclusions Fulminant liver failure developed after the ingestion of food contaminated with the B. cereus emetic toxin, The toxin inhibits hepatic mitochondrial fatty-acid oxidation, indicating that it caused liver failure in this patient. (C) 1997, Massachusetts Medical Society.