Cohen S H, Tang Y J, Silva J
Department of Internal Medicine, Division of Infectious and Immunologic Diseases, University of California, Davis Medical Center, Sacramento, CA 95817, USA.
J Infect Dis. 2000 Feb;181(2):659-63. doi: 10.1086/315248.
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.
艰难梭菌毒素A和B（tcdA和tcdB）的基因是一个19.6 kb致病位点（PaLoc）的一部分，该位点包括tcdD、tcdE和tcdC基因。为了确定艰难梭菌PaLoc在产毒菌株中是否是一个稳定且保守的遗传单位，采用多重聚合酶链反应分析了50株产毒菌株、39株无毒菌株和2株毒素缺陷型分离株。在产毒菌株中鉴定出了tcdA - E各自的扩增子；这些在无毒菌株中不存在。艰难梭菌P - 829至少缺失了tcdD、tcdB、tcdE和tcdC的一个片段，但tcdA存在。艰难梭菌8864的tcdA和tcdC基因存在缺失。这些数据表明，PaLoc在产毒艰难梭菌中高度稳定，无毒分离株缺乏该单位，且PaLoc有缺陷的分离株仍可引起临床疾病。需要进一步研究来确定各个基因在艰难梭菌相关性腹泻发病机制中的作用。
