Salmonella enterica serovar senftenberg human clinical isolates lacking SPI-1
Salmonella enterica serovar senftenberg human clinical isolates lacking SPI-1
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DOI：
10.1128/jcm.01255-07
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发表时间：
2008-04-01
影响因子：
9.4
通讯作者：
Finlay, B. Brett
中科院分区：
文献类型：
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作者：
Hu, Qinghua;Coburn, Bryan;Finlay, B. Brett
非伤寒沙门氏菌在世界范围内引起胃肠道疾病。沙门氏菌肠道致病性的流行理论是，细菌侵入肠上皮是必不可少的毒力，这需要毒力相关的基因组区域沙门氏菌致病岛1（SPI-1）。最近对沙门氏菌感染模型的研究表明，小鼠和奶牛的小肠结肠炎和腹泻可以独立于SPI-1发生。在这项研究中，我们试图确认是否两个S。肠道血清型森夫滕贝格临床分离株缺乏SPI-1功能所必需的基因。分离到2株临床菌株，经鉴定为S.采用常规方法、脉冲场凝胶电泳和多位点序列分型，从中国广东省深圳市发生的一起食源性疾病暴发疫情中的4份粪便样本中分离出肠道血清型森夫滕贝格。排除了与其他潜在细菌或常见病毒合并感染的可能性。通过PCR和Southern印迹分析两个分离物的invA、sipA、ssaR、sifA和sopE 2的存在，然后通过PCR和fhlA-hilA、hilA-spaP和spaP-invH的长距离PCR和Southern印迹分析测定SPI-1的存在。还从两个临床分离物中扩增了覆盖SPI-1的5'和3'侧翼的从fhlA到mutS的长距离PCR片段并测序。此外，两种临床分离株进行了肠侵袭性体外测定。还检查了鼠感染模型。经生化试验和血清学分型证实，这两株临床分离株均为沙门氏菌。肠道血清型森夫滕贝格。然而，它们缺乏对SPI-1功能至关重要的基因，但含有SPI-2基因，并且对于培养的肠上皮细胞的侵袭是减弱的。结论：临床S.从食源性疾病爆发中分离的肠道血清型森夫滕贝格菌株缺乏侵袭相关基因座SPI-1，表明SPI-1不是人类胃肠炎所必需的。
Nontyphoidal Salmonella species cause gastrointestinal disease worldwide. The prevailing theory of Salmonella enteropathogenesis is that bacterial invasion of the intestinal epithelium is essential for virulence and that this requires the virulence-associated genomic region Salmonella pathogenicity island 1 (SPI-1). Recent studies of Salmonella enterica infection models have demonstrated that enterocolitis and diarrhea in mice and cows can occur independently of SPI-1. In this study, we sought to confirm whether two S. enterica serovar Senftenberg clinical isolates lacked genes essential for SPI-1 function. Two clinical strains were isolated and identified as being S. enterica serovar Senftenberg from four stool samples from a food-borne disease outbreak affecting seven individuals in Shenzhen, Guangdong Province, China, using conventional methods, pulsed-field gel electrophoresis and multilocus sequence typing. The possibility of coinfection with other potential bacteria or usual viruses was excluded. Two isolates were analyzed for the presence of invA, sipA, ssaR, sifA, and sopE2 by PCR and Southern blotting and were then assayed for the presence of SPI-1 by PCR and long-range PCR for fhlA-hilA, hilA-spaP, and spaP-invH and Southern blot analysis. A long-range PCR fragment from fhlA to mutS covering the 5' and 3' flanks of SPI-1 was also amplified from the two clinical isolates and sequenced. In addition, the two clinical isolates were assayed for enteroinvasiveness in vitro. Murine infection models were also examined. Biochemical tests and serotyping confirmed that the two clinical isolates are S. enterica serovar Senftenberg. However, they lacked genes critical for SPI-1 function but contained SPI-2 genes and were attenuated for the invasion of cultured intestinal epithelial cells. In conclusion, clinical S. enterica serovar Senftenberg strains isolated from a food-borne disease outbreak lack the invasion-associated locus SPI-1, indicating that SPI-1 is not essential for human gastroenteritis.