Brooks John T, Sowers Evangeline G, Wells Joy G, Greene Katherine D, Griffin Patricia M, Hoekstra Robert M, Strockbine Nancy A
Foodborne and Diarrheal Diseases Branch, Division of Bacterial and Mycotic Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia 30333, USA.
J Infect Dis. 2005 Oct 15;192(8):1422-9. doi: 10.1086/466536. Epub 2005 Sep 14.
Shiga toxin-producing Escherichia coli (STEC) O157:H7 is a well-recognized cause of bloody diarrhea and hemolytic-uremic syndrome (HUS). Non-O157 STEC contribute to this burden of illness but have been underrecognized as a result of diagnostic limitations and inadequate surveillance.
Between 1983 and 2002, 43 state public health laboratories submitted 940 human non-O157 STEC isolates from persons with sporadic illnesses to the Centers for Diseases Control and Prevention reference laboratory for confirmation and serotyping.
The most common serogroups were O26 (22%), O111 (16%), O103 (12%), O121 (8%), O45 (7%), and O145 (5%). Non-O157 STEC infections were most frequent during the summer and among young persons (median age, 12 years; interquartile range, 3-37 years). Virulence gene profiles were as follows: 61% stx(1) but not stx(2); 22% stx(2) but not stx(1); 17% both stx(1) and stx(2); 84% intimin (eae); and 86% enterohemolysin (E-hly). stx(2) was strongly associated with an increased risk of HUS, and eae was strongly associated with an increased risk of bloody diarrhea. STEC O111 accounted for most cases of HUS and was also the cause of 3 of 7 non-O157 STEC outbreaks reported in the United States.
Non-O157 STEC can cause severe illness that is comparable to the illness caused by STEC O157. Strains that produce Shiga toxin 2 are much more likely to cause HUS than are those that produce Shiga toxin 1 alone. Improving surveillance will more fully elucidate the incidence and pathological spectrum of these emerging agents. These efforts require increased clinical suspicion, improved clinical laboratory isolation, and continued serotyping of isolates in public health laboratories.
产志贺毒素大肠杆菌（STEC）O157:H7是血性腹泻和溶血尿毒综合征（HUS）的一个公认病因。非O157 STEC也导致了这一疾病负担，但由于诊断限制和监测不足，一直未得到充分认识。
1983年至2002年间，43个州的公共卫生实验室将940株来自散发病例患者的人类非O157 STEC分离株提交给疾病控制和预防中心参考实验室进行确认和血清分型。
最常见的血清群为O26（22%）、O111（16%）、O103（12%）、O121（8%）、O45（7%）和O145（5%）。非O157 STEC感染在夏季最为常见，且多见于年轻人（中位年龄12岁；四分位间距3 - 37岁）。毒力基因谱如下：61%为stx(1)而非stx(2)；22%为stx(2)而非stx(1)；17%同时含有stx(1)和stx(2)；84%含有intimin（eae）；86%含有肠溶血素（E-hly）。stx(2)与HUS风险增加密切相关，eae与血性腹泻风险增加密切相关。STEC O111占大多数HUS病例，也是美国报告的7起非O157 STEC暴发中3起的病因。
非O157 STEC可导致与STEC O157所致疾病相当的严重疾病。产志贺毒素2的菌株比仅产志贺毒素1的菌株更易引发HUS。加强监测将更全面地阐明这些新出现病原体的发病率和病理谱。这些工作需要提高临床怀疑度、改进临床实验室分离方法，并持续在公共卫生实验室对分离株进行血清分型。
