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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
by
Boyd, Dave
, Alfa, Michelle J
, Mulvey, Michael R
, Murray, Ruth
, Levett, Paul N
in
Amino Acid Sequence
/ Bacterial Proteins - genetics
/ Bacterial Proteins - metabolism
/ Bacterial toxins
/ Bacterial Toxins - metabolism
/ Bacterial Typing Techniques
/ Caco-2 Cells
/ Clostridium difficile
/ Clostridium difficile - classification
/ Clostridium difficile - genetics
/ Clostridium difficile - growth & development
/ DNA, Bacterial - genetics
/ Enterotoxins - metabolism
/ Gene Expression Regulation, Bacterial
/ Genetic aspects
/ Health aspects
/ Humans
/ Identification and classification
/ Molecular Sequence Data
/ Mutation
/ Production processes
/ Repressor Proteins - genetics
/ Sequence Analysis, DNA
2009
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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
by
Boyd, Dave
, Alfa, Michelle J
, Mulvey, Michael R
, Murray, Ruth
, Levett, Paul N
in
Amino Acid Sequence
/ Bacterial Proteins - genetics
/ Bacterial Proteins - metabolism
/ Bacterial toxins
/ Bacterial Toxins - metabolism
/ Bacterial Typing Techniques
/ Caco-2 Cells
/ Clostridium difficile
/ Clostridium difficile - classification
/ Clostridium difficile - genetics
/ Clostridium difficile - growth & development
/ DNA, Bacterial - genetics
/ Enterotoxins - metabolism
/ Gene Expression Regulation, Bacterial
/ Genetic aspects
/ Health aspects
/ Humans
/ Identification and classification
/ Molecular Sequence Data
/ Mutation
/ Production processes
/ Repressor Proteins - genetics
/ Sequence Analysis, DNA
2009
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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
by
Boyd, Dave
, Alfa, Michelle J
, Mulvey, Michael R
, Murray, Ruth
, Levett, Paul N
in
Amino Acid Sequence
/ Bacterial Proteins - genetics
/ Bacterial Proteins - metabolism
/ Bacterial toxins
/ Bacterial Toxins - metabolism
/ Bacterial Typing Techniques
/ Caco-2 Cells
/ Clostridium difficile
/ Clostridium difficile - classification
/ Clostridium difficile - genetics
/ Clostridium difficile - growth & development
/ DNA, Bacterial - genetics
/ Enterotoxins - metabolism
/ Gene Expression Regulation, Bacterial
/ Genetic aspects
/ Health aspects
/ Humans
/ Identification and classification
/ Molecular Sequence Data
/ Mutation
/ Production processes
/ Repressor Proteins - genetics
/ Sequence Analysis, DNA
2009
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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
Journal 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
2009
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Overview
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.
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.
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.
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.
Publisher
BioMed Central Ltd,BioMed Central,BMC
Subject
/ Bacterial Proteins - genetics
/ Bacterial Proteins - metabolism
/ Bacterial Toxins - metabolism
/ Clostridium difficile - classification
/ Clostridium difficile - genetics
/ Clostridium difficile - growth & development
/ Gene Expression Regulation, Bacterial
/ Humans
/ Identification and classification
/ Mutation
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