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Background  The increased severity of disease associated with the NAP1 strain of  Clostridium difficile  has been attributed to mutations to the  tcdC  gene which codes for a negative regulator of toxin production. To assess the role of hyper-production of Toxins A and B in clinical isolates of  Clostridium difficile , two NAP1-related and five NAP1 non-related strains were compared.    Methods  Sequencing was performed on  tcdC ,  tcdR , and  tcdE  to determine if there were differences that might account for hyper-production of Toxin A and Toxin B in NAP1-related strains. Biological activity of Toxin B was evaluated using the HFF cell CPE assay and Toxin A biological activity was assessed using the Caco-2 Trans-membrane resistance assay.    Results  Our results confirm that Toxin A and Toxin B production in NAP1-related strains and ATCC 43255 occurs earlier in the exponential growth phase compared to most NAP1-nonrelated clinical isolates. Despite the hyper-production observed in ATCC 43255 it had no mutations in  tcdC ,  tcdR  or  tcdE . Analysis of the other clinical isolates indicated that the kinetics and ultimate final concentration of Toxin A and B did not correlate with the presence or lack of alterations in  tcdC ,  tcdR  or  tcdE .    Conclusion  Our data do not support a direct role for alterations in the  tcdC  gene as a predictor of hyperproduction of Toxin A and B in NAP1-related strains.

bmc infectious diseases

Truncation in the tcdC region of the Clostridium difficilePathLoc of clinical isolates does not predict increased biological activity of Toxin B or Toxin A