Analysis of the pathogenicity locus in Clostridium difficile strains
Analysis of the pathogenicity locus in Clostridium difficile strains
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DOI：
10.1086/315248
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发表时间：
2000-02-01
影响因子：
6.4
通讯作者：
Silva, J
中科院分区：
文献类型：
--
作者：
Cohen, SH;Tang, YJ;Silva, J
艰难梭菌毒素A和B的基因（tcdA和tcdB）是19.6 kb致病性位点（PaLoc）的一部分，其中包括tcdD、tcdE和tcdC基因。为了确定艰难梭菌PaLoc是否是产毒菌株中稳定且保守的遗传单位，采用多重聚合酶链反应对50株产毒、39株非产毒和2株毒缺陷菌株进行了分析。在产毒菌株中分别鉴定出tcdA-E扩增子；这些在非产毒菌株中不存在。艰难梭菌P-829至少缺乏tcdD、tcdB、tcdE和tcdC的片段，但tcdA存在。艰难梭菌8864有tcdA和tcdC基因缺失。这些数据表明，PaLoc在产毒C中高度稳定，难辨菌、非产毒菌株缺乏该单位，PaLoc有缺陷的菌株仍可引起临床疾病。需要进一步的研究来确定单个基因在艰难梭菌相关性腹泻发病机制中的作用。
The genes for Clostridium difficile toxins A and B (tcdA and tcdB) are part of a 19.6-kb pathogenicity locus (PaLoc) that includes the genes tcdD, tcdE, and tcdC. To determine whether the C. difficile PaLoc is a stable and conserved genetic unit in toxigenic strains, a multiplex polymerase chain reaction was used to analyze 50 toxigenic, 39 nontoxigenic, and 2 toxin-defective isolates. The respective amplicons were identified for tcdA-E in the toxigenic isolates; these were absent in the nontoxigenic isolates. C. difficile P-829 lacked at least a fragment of tcdD, tcdB, tcdE, and tcdC, but tcdA was present. C. difficile 8864 had deletions in the tcdA and tcdC genes. These data suggest that the PaLoc is highly stable in toxigenic C, difficile, nontoxigenic isolates lack the unit, and isolates with a defective PaLoc can still cause clinical disease. Further studies are needed to define the role of individual genes in the pathogenesis of C. difficile-associated diarrhea.