The main virulence factors of the enteropathogenic C. difficile are the two large clostridial toxins, toxin A (TcdA) and toxin B (TcdB). These toxins are glycosyltransferases that inactivate Rho, Rac and Cdc42, thereby disrupting the cytoskeleton and tight junctions of the cells, resulting in apoptosis [10] . This induces an inflammatory response and degradation of the intestinal epithelial cell layer. Besides the genes encoding these toxins (tcdA and tcdB), the pathogenicity locus (PaLoc) also contains genes encoding a sigma factor (tcdR) and a putative anti-sigma factor (tcdC) [11] [12] [13] . In between the toxin genes the tcdE gene is situated, which encodes a putative holin protein [14] . Interestingly, both hypervirulent Types 027 and 078 have been shown to contain mutations in the tcdC gene, encoding the putative negative regulator of toxin gene transcription, and this has been proposed as a possible explanation for their increased virulence [8, 15] .