This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow An author's correction has been published
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Curry, S. R.
Right arrow Articles by Harrison, L. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Curry, S. R.
Right arrow Articles by Harrison, L. H.

 Previous Article  |  Next Article 

Journal of Clinical Microbiology, January 2007, p. 215-221, Vol. 45, No. 1
0095-1137/07/$08.00+0     doi:10.1128/JCM.01599-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

tcdC Genotypes Associated with Severe TcdC Truncation in an Epidemic Clone and Other Strains of Clostridium difficile{triangledown}

Scott R. Curry,1 Jane W. Marsh,1,4 Carlene A. Muto,1,2 Mary M. O'Leary,2,4 A. William Pasculle,1,3 and Lee H. Harrison1,4*

Division of Infectious Diseases, Department of Medicine, University of Pittsburgh School of Medicine,1 Division of Hospital Epidemiology and Infection Control and Division of Infectious Diseases, University of Pittsburgh Medical Center, Presbyterian Campus,2 Division of Microbiology, Department of Pathology, University of Pittsburgh School of Medicine,3 Infectious Diseases Epidemiology Research Unit, University of Pittsburgh School of Medicine and Graduate School of Public Health, Pittsburgh, Pennsylvania 152614

Received 2 August 2006/ Returned for modification 5 September 2006/ Accepted 29 September 2006

Severe Clostridium difficile associated disease is associated with outbreaks of the recently described BI/NAP1 epidemic clone. This clone is characterized by an 18-bp deletion in the tcdC gene and increased production of toxins A and B in vitro. TcdC is a putative negative regulator of toxin A&B production. We characterized tcdC genotypes from a collection of C. difficile isolates from a hospital that experienced an outbreak caused by the BI/NAP1 epidemic clone. Sequence analysis of tcdC was performed on DNA samples isolated from 199 toxigenic C. difficile isolates (31% BI/NAP1) from 2001 and 2005. Sequences obtained from 36 (18.6%) isolates predicted wild-type TcdC (232 amino acid residues), whereas 12 (6.1%) isolates had tcdC genotypes with previously described 18- or 39-bp deletions. The remaining isolates comprised 15 unique genotypes. Of these, 5 genotypes contain 18- or 36-bp deletions. Of these five genotypes, one is characterized by a single nucleotide deletion at position 117 resulting in a frameshift that introduces a stop codon at position 196, truncating the predicted TcdC to 65 amino acid residues. All 62 of the isolates in this collection comprising the epidemic clone are characterized by this genotype. This result suggests that severe truncation of TcdC is responsible for the increased toxin production observed in strains belonging to the BI/NAP1 clone and that the 18-bp deletion is probably irrelevant to TcdC function. Further investigations are required to determine the effect of this and other tcdC genotypes on toxin production and clinical disease.

* Corresponding author. Mailing address: University of Pittsburgh Graduate School of Public Health, 521 Parran Hall, 130 DeSoto St., Pittsburgh, PA 15261. Phone: (412) 624-3137. Fax: (412) 624-3120. E-mail: lharriso{at}edc.pitt.edu.

{triangledown} Published ahead of print on 11 October 2006.

Journal of Clinical Microbiology, January 2007, p. 215-221, Vol. 45, No. 1
0095-1137/07/$08.00+0     doi:10.1128/JCM.01599-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Wroblewski, D., Hannett, G. E., Bopp, D. J., Dumyati, G. K., Halse, T. A., Dumas, N. B., Musser, K. A. (2009). Rapid Molecular Characterization of Clostridium difficile and Assessment of Populations of C. difficile in Stool Specimens. J. Clin. Microbiol. 47: 2142-2148 [Abstract] [Full Text]  
  • Janvilisri, T., Scaria, J., Thompson, A. D., Nicholson, A., Limbago, B. M., Arroyo, L. G., Songer, J. G., Grohn, Y. T., Chang, Y.-F. (2009). Microarray Identification of Clostridium difficile Core Components and Divergent Regions Associated with Host Origin. J. Bacteriol. 191: 3881-3891 [Abstract] [Full Text]  
  • Ochsner, U. A., Bell, S. J., O'Leary, A. L., Hoang, T., Stone, K. C., Young, C. L., Critchley, I. A., Janjic, N. (2009). Inhibitory effect of REP3123 on toxin and spore formation in Clostridium difficile, and in vivo efficacy in a hamster gastrointestinal infection model. J Antimicrob Chemother 63: 964-971 [Abstract] [Full Text]  
  • Bouvet, P. J. M., Popoff, M. R. (2008). Genetic Relatedness of Clostridium difficile Isolates from Various Origins Determined by Triple-Locus Sequence Analysis Based on Toxin Regulatory Genes tcdC, tcdR, and cdtR. J. Clin. Microbiol. 46: 3703-3713 [Abstract] [Full Text]  
  • Martin, H., Willey, B., Low, D. E., Staempfli, H. R., McGeer, A., Boerlin, P., Mulvey, M., Weese, J. S. (2008). Characterization of Clostridium difficile Strains Isolated from Patients in Ontario, Canada, from 2004 to 2006. J. Clin. Microbiol. 46: 2999-3004 [Abstract] [Full Text]  
  • Hinkson, P. L., Dinardo, C., DeCiero, D., Klinger, J. D., Barker, R. H. Jr. (2008). Tolevamer, an Anionic Polymer, Neutralizes Toxins Produced by the BI/027 Strains of Clostridium difficile. Antimicrob. Agents Chemother. 52: 2190-2195 [Abstract] [Full Text]  
  • Sloan, L. M., Duresko, B. J., Gustafson, D. R., Rosenblatt, J. E. (2008). Comparison of Real-Time PCR for Detection of the tcdC Gene with Four Toxin Immunoassays and Culture in Diagnosis of Clostridium difficile Infection. J. Clin. Microbiol. 46: 1996-2001 [Abstract] [Full Text]  
  • Stabler, R. A., Dawson, L. F., Phua, L. T. H., Wren, B. W. (2008). Comparative analysis of BI/NAP1/027 hypervirulent strains reveals novel toxin B-encoding gene (tcdB) sequences. J Med Microbiol 57: 771-775 [Abstract] [Full Text]  
  • Samie, A., Obi, C. L., Franasiak, J., Archbald-Pannone, L., Bessong, P. O., Alcantara-Warren, C., Guerrant, R. L. (2008). PCR Detection of Clostridium difficile Triose Phosphate Isomerase (tpi), Toxin A (tcdA), Toxin B (tcdB), Binary Toxin (cdtA, cdtB), and tcdC Genes in Vhembe District, South Africa. Am J Trop Med Hyg 78: 577-585 [Abstract] [Full Text]  
  • Akerlund, T., Persson, I., Unemo, M., Noren, T., Svenungsson, B., Wullt, M., Burman, L. G. (2008). Increased Sporulation Rate of Epidemic Clostridium difficile Type 027/NAP1. J. Clin. Microbiol. 46: 1530-1533 [Abstract] [Full Text]  
  • Freeman, J., Baines, S. D., Saxton, K., Wilcox, M. H. (2007). Effect of metronidazole on growth and toxin production by epidemic Clostridium difficile PCR ribotypes 001 and 027 in a human gut model. J Antimicrob Chemother 60: 83-91 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»