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

doi:10.1186/1471-2334-9-103

BMC Infectious Diseases

Volume 9

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Murray R
Boyd D
Levett PN
Mulvey MR
Alfa MJ

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Research article

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

Ruth Murray¹^,4^* , Dave Boyd²^* , Paul N Levett³^* , Michael R Mulvey²^* and Michelle J Alfa⁴

¹St. Boniface Research Centre, Winnipeg, MB, Canada

²Public Health Agency of Canada, Winnipeg, MB, Canada

³Public Health Agency of Canada, Saskatchewan, Canada

⁴Department of Medical Microbiology, University of Manitoba, Winnipeg, MB, Canada

author email corresponding author email* Contributed equally

BMC Infectious Diseases 2009, 9:103doi:10.1186/1471-2334-9-103


Published:	28 June 2009

Abstract

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.