Naik Sandhia, Smith Fabienne, Ho John, Croft Nicholas M, Domizio Paola, Price Elisabeth, Sanderson Ian R, Meadows Nigel J
Department of Paediatric Gastroenterology, Barts and the London NHS Trust, London, United Kingdom.
Clin Gastroenterol Hepatol. 2008 Feb;6(2):251-4. doi: 10.1016/j.cgh.2007.09.004. Epub 2007 Dec 11.
BACKGROUND & AIMS: Staphylococcus aureus is recognized to produce toxins A-E and toxic shock syndrome toxin-1 associated with food poisoning and toxic shock syndrome. Enterotoxins G and I co-exist in the same S aureus strains (staphylococcal enterotoxin G and staphylococcal enterotoxin I) and are implicated in scarlet fever and toxic shock. We report these enterotoxins as causative agents of 2 cases of neonatal intractable diarrhea with enteropathy.
We used a note review for this study. Stool culture, multiplex polymerase chain reaction for enterotoxin, duodenal biopsy specimens for H&E, periodic acid-Schiff staining, and electron microscopy were used.
Infant 1 had diarrhea from age 2 weeks and was referred at age 5 weeks with weight less than the 0.4th percentile. Infant 2 was referred at age 7 weeks with 4 weeks' of diarrhea, weight less than the 0.4th percentile. Both infants were severely malnourished. Elemental feeds were not tolerated and total parenteral nutrition was required. S aureus producing staphylococcal enterotoxin G and staphylococcal enterotoxin I was isolated in stools from both infants. Clinical improvement occurred after intravenous flucloxacillin and parenteral nutrition. Histology showed subtotal villous atrophy (H&E) with abnormal brush border (periodic acid-Schiff). Electron microscopy showed severe microvilli destruction, dilated mitochondria, and lysosomes containing cellular debris. Repeat histology was normal in infant 2, age 3 months, off parenteral nutrition, showed return to normal. Currently, both infants are 2 years of age and are thriving on a normal diet.
Staphylococcal enterotoxin G- and I-induced enteropathy is a life-threatening condition, causing reversible disruption of enterocyte ultrastructure that responds well to supportive treatment with flucloxacillin and parenteral nutrition This condition should be a differential diagnosis of neonatal early onset diarrhea.
金黄色葡萄球菌可产生与食物中毒和中毒性休克综合征相关的A-E毒素及中毒性休克综合征毒素-1。肠毒素G和I共存于同一金黄色葡萄球菌菌株中（葡萄球菌肠毒素G和葡萄球菌肠毒素I），与猩红热和中毒性休克有关。我们报告这两种肠毒素是2例新生儿难治性腹泻伴肠病的致病因素。
本研究采用病例回顾。进行了粪便培养、肠毒素多重聚合酶链反应、十二指肠活检标本的苏木精-伊红染色、过碘酸-雪夫染色及电子显微镜检查。
婴儿1在2周龄时出现腹泻，5周龄时因体重低于第0.4百分位数而转诊。婴儿2在7周龄时因腹泻4周、体重低于第0.4百分位数而转诊。两名婴儿均严重营养不良。不能耐受要素饮食，需要全胃肠外营养。在两名婴儿的粪便中均分离出产生葡萄球菌肠毒素G和葡萄球菌肠毒素I的金黄色葡萄球菌。静脉注射氟氯西林和胃肠外营养后临床症状改善。组织学检查显示绒毛大部萎缩（苏木精-伊红染色），刷状缘异常（过碘酸-雪夫染色）。电子显微镜检查显示微绒毛严重破坏、线粒体扩张以及含有细胞碎片的溶酶体。婴儿2在3个月龄时停用胃肠外营养，重复组织学检查显示恢复正常。目前，两名婴儿均2岁，正常饮食，生长良好。
葡萄球菌肠毒素G和I诱导的肠病是一种危及生命的疾病，可导致肠细胞超微结构的可逆性破坏，对氟氯西林和胃肠外营养支持治疗反应良好。这种疾病应作为新生儿早发性腹泻的鉴别诊断之一。
