Phenotypic characterization of enterotoxigenic Clostridium perfringens isolates from non-foodborne human gastrointestinal diseases
Phenotypic characterization of enterotoxigenic Clostridium perfringens isolates from non-foodborne human gastrointestinal diseases
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DOI：
10.1006/anae.1998.0152
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发表时间：
1998-04-01
期刊：
影响因子：
2.3
通讯作者：
McClane, BA
中科院分区：
文献类型：
--
作者：
Collie, RE;Kokai-Kun, JF;McClane, BA
产气荚膜梭菌肠毒素（CPE）被认为是A型产气荚膜梭菌食物中毒和几种非食源性人类胃肠道（GI）疾病（包括抗生素相关性腹泻（AAD）和散发性腹泻（SPOR））的重要毒力因子。最近的研究揭示了来自不同疾病来源的cpe阳性分离株之间的基因型差异，大多数或全部食物中毒分离株携带染色体cpe，而大多数或全部非食源性人类胃肠道疾病分离株携带外源性cpe。为了评估这些基因型差异是否会引起表型效应，从而影响cpe相关的非食源性人类胃肠道疾病的发病机制，本研究对SPOR和AAD分离株进行了表型表征。所有CPE阳性的非食源性疾病分离株被发现以孢子相关的方式表达CPE。结果表明，由AAD和SPOR分离株制备的CPE与由食物中毒分离株制备的CPE具有相同的推导氨基酸序列和毒性。所有被调查的非食源性人类胃肠道疾病分离株被发现归类为A型产气荚膜杆菌，因为它们产生毒素，但不产生β、iota或epsilon毒素。最后，在调查的非食源性人类胃肠道疾病分离株之间没有发现一致的克隆关系。由于根据检测标准，本研究检测的所有非食源性人类胃肠道疾病分离株在表型上与食物中毒分离株相似，因此目前的结果证实，检测的AAD和SPOR分离株具有肠致病性潜力。然而，鉴于本研究已证实的食物中毒、AAD和SPOR分离株之间的表型相似性，尚不清楚为什么非食源性人类胃肠道疾病的症状通常比A型产气荚膜荚膜杆菌食物中毒更严重、持续时间更长。(C) 1998学术出版社。
Clostridium perfringens enterotoxin (CPE) has been implicated as an important virulence factor in C. perfringens type A food poisoning and several non-foodborne human gastrointestinal (GI) illnesses, including antibiotic-associated diarrhea (AAD) and sporadic diarrhea (SPOR). Recent studies have revealed genotypic differences between cpe-positive isolates originating from different disease sources, with most, or all, food poisoning isolates carrying a chomosomal cpe and most, or all, non-foodborne human GI disease isolates carrying an episomal cpe. To evaluate whether these genotypic differences cause phenotypic effects that could influence the pathogenesis of CPE-associated non-foodborne human GI illnesses, a collection of SPOR and AAD isolates has been phenotypically characterized in the current study. All cpe-positive non-foodborne disease isolates examined were found to express CPE in a sporulation-associated manner. The CPE made by these AAD and SPOR isolates was shown to have the same deduced amino acid sequence and toxicity as the classical CPE made by food poisoning isolates. All of the surveyed non-foodborne human GI disease isolates were found to classify as type A C. perfringens, since they produce a toxin, but not beta, iota, or epsilon toxins. Finally, no consistent clonal relationships were detected between the surveyed non-foodborne human GI disease isolates. Since, by the criteria examined, all non-foodborne human GI disease isolates examined in this study appear to be phenotypically similar to food poisoning isolates, the current results confirm that the examined AAD and SPOR isolates have enteropathogenic potential. However, given the phenotypic similarities between food poisoning, AAD, and SPOR isolates that have been demonstrated in this study, it remains unclear why the symptomology of non-foodborne human GI diseases is typically more severe and longer-lasting than that of C. perfringens type A food poisoning. (C) 1998 Academic Press.