Enterohemorrhagic Escherichia coli O157: H7 infection

S. Shinoda, Shigeo Yamamoto, K. Tomochika, S. Miyoshi
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引用次数: 3

Abstract

The first recognized outbreaks of hemorrhagic colitis occurred in 1982 in the United State and its etiologic agent was identified to be Escherichia coli O157 : H7, a serotype not previously associated with diseases in humans. In Japan, isolates of the serotype O157 : H7 from contaminated drinking water were first implicated in an outbreak occurred in 1990 in a kindergarten of the Saitama Prefecture, and at least other 12 such outbreaks have been recorded in 1993-1995. In the year 1996, unprecedentedly large outbreaks and many sporadic cases of disease caused by E. coli O157 : H7 occurred in various parts of Japan, affecting more than 9000 people in total (11 deaths). In most cases, however, the ultimate source of the infection could not be traced. Although many different serotypes of E. coli, which are collectively referred to as enterohemorrhagic E. coli (EHEC), were found to cause bloody diarrhea, the serotype O157 : H7 has been recognized worldwide as the pathogen associated most frequently with serious complications known as hemolytic colitis and hemolytic uremic syndrome. E. coli O157 : H7 is characteristic of a low infectious dose, on the order of a few hundred organisms, which contributes to the spread of the infection in outbreak situations. Cattle are considered to be the major reservoir of EHEC including O157 : H7. EHEC strains produce at least two immunologically distinct cytotoxins that closely resemble the Shiga toxin produced by the Shigella dysenteriae type 1 strains. These toxins (called Shiga-like toxins or Vero toxins) appear to be responsible for causing many pathological effects associated with EHEC infections. However, how the toxins move from the intestinal tract lumen to the sites where they damage the kidney remains to be evaluated. Moreover, there are some doubts about the value of antibiotic therapy in such infections because of the observation that some antibiotics can increase the toxin expression in vitro and because of the concern that EHEC which are lysing due to their actions in the gastrointestinal tract lumen may actually release more toxin than do intact bacterial cells. Unique biochemical characteristics of E. coli O157 : H7-it ferments sorbitol very slowly and usually does not make β-glucuronidase- are used to differentiate this strain from other enteric E. coli strains. Alternative methods based on the detection of the toxins themselves by enzyme immunoassay are employed in parallel. This review describes the current understanding of the infectious disease caused by E. coli O157 : H7, with an emphasis on the main diagnostic tests and epidemiology for this serotype and the role of the toxins in pathogenesis.
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肠出血性大肠杆菌O157: H7感染
第一次确认的出血性结肠炎暴发发生在1982年的美国,其病原被确定为大肠杆菌O157: H7,这是一种以前与人类疾病无关的血清型。在日本,从受污染的饮用水中分离出的血清型O157: H7最初与1990年在埼玉县一所幼儿园发生的疫情有关,1993-1995年期间至少记录了其他12次此类疫情。1996年,日本各地发生了由大肠杆菌O157: H7引起的空前大规模疫情和许多散发病例,总共影响了9000多人(11人死亡)。然而,在大多数情况下,无法追踪感染的最终来源。虽然发现许多不同血清型大肠杆菌(统称为肠出血性大肠杆菌)可引起血性腹泻,但世界范围内公认O157: H7血清型是与溶血性结肠炎和溶血性尿毒症综合征等严重并发症最常相关的病原体。大肠杆菌O157: H7的特点是感染剂量低,大约只有几百个生物体,这有助于在疫情情况下感染的传播。牛被认为是肠出血性大肠杆菌的主要宿主,包括O157: H7。肠出血性大肠杆菌菌株产生至少两种免疫学上不同的细胞毒素,它们与志贺氏痢疾杆菌1型菌株产生的志贺毒素非常相似。这些毒素(称为志贺样毒素或维罗毒素)似乎是导致肠出血性大肠杆菌感染相关的许多病理效应的原因。然而,毒素如何从肠道腔转移到损害肾脏的部位仍有待评估。此外,由于观察到一些抗生素可以增加体外毒素表达,以及由于肠出血性大肠杆菌在胃肠道腔内的作用而溶解,实际上可能比完整的细菌细胞释放更多的毒素,因此对抗生素治疗在此类感染中的价值存在一些怀疑。大肠杆菌O157: h7的独特生化特性——它发酵山梨醇非常缓慢,通常不产生β-葡萄糖醛酸酶——被用来区分该菌株与其他肠道大肠杆菌菌株。基于酶免疫测定法检测毒素本身的替代方法被并行采用。本文综述了目前对大肠杆菌O157: H7引起的传染病的认识,重点介绍了该血清型的主要诊断试验和流行病学以及毒素在发病机制中的作用。
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