Transcription Analysis of the Genes <i>tcdA‐E</i> of the Pathogenicity Locus of <i>Clostridium Difficile</i>

Hundsberger, Thomas; Braun, Veil; Weidmann, Manfred; Leukel, Petra; Sauerborn, Markus; Eichel‐Streiber, Christoph von

doi:10.1111/j.1432-1033.1997.t01-1-00735.x

Cited by 185 publications

(202 citation statements)

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“…(iv) Similar to tcdR, the negative regulator of toxin expression tcdC had a putative CodY binding site at its promoter and was induced together with the other PaLoc genes in the C. difficile codY mutant (Dineen et al, 2007). Although the level of tcdC induction was apparently lower than for the other PaLoc genes, it was not consistent with the opposite transcription pattern of tcdC found in C. difficile strain VPI 10463 (Hundsberger et al, 1997). We observed only small changes of tcdC mRNA level in strain VPI 10463 during induction of tcdA and tcdR (Fig.…”

Section: Discussionmentioning

confidence: 42%

Induction of toxins in Clostridium difficile is associated with dramatic changes of its metabolism

2008

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Certain amino acids, and cysteine in particular, promptly blocked toxin expression in Clostridium difficile strain VPI 10463 when added to late-exponential-phase peptone-yeast cultures, i.e. prior to normal induction of toxins A and B. Glucose reduced toxin yields by 80-fold, but only when supplemented at inoculation. Forty upregulated C. difficile proteins were identified during maximum toxin expression, and most of these were enzymes involved in energy exchange, e.g. succinate, CO/folate and butyrate metabolism. Transcription of tcdA (toxin operon) and folD (CO/ folate operon) was induced by 20-and 10-fold, respectively, and with strikingly similar kinetics between OD 0.8 and 1.2. The sigma factors tcdR and sigH were upregulated simultaneously with tcdA and folD (3.5-fold increase of mRNA level), whereas transcription of tcdC, codY, sigB and sigL showed little or no correlation with that of tcdA and folD. The results suggest a connection between toxin expression, alternative energy metabolism and initial sporulation events in C. difficile.

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Section: Discussionmentioning

confidence: 42%

Induction of toxins in Clostridium difficile is associated with dramatic changes of its metabolism

2008

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“…Also encoded are three accessory genes: two putative regulatory genes (tcdC and tcdR) and a holin-like gene (tcdE) (Hundsberger et al, 1997) required for toxin-release (Govind and Dupuy, 2012) (Figure 3). Also downstream of the tcdE is a partial N-acetyl-muramoyl alanine amidase of unknown significance (Monot et al, 2011).…”

Section: Description Of Palocmentioning

confidence: 99%

Clostridium difficile infection: Evolution, phylogeny and molecular epidemiology

Elliott

Androga

Knight

et al. 2017

Infection, Genetics and Evolution

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Over the recent decades, Clostridium difficile infection (CDI) has emerged as a global public health threat. Despite growing attention, C. difficile remains a poorly understood pathogen, however, the exquisite sensitivity offered by next generation sequencing (NGS) technology has enabled analysis of the genome of C. difficile, giving us access to massive genomic data on factors such as virulence, evolution, and genetic relatedness within C. difficile groups. NGS has also demonstrated excellence in investigations of outbreaks and disease transmission, in both small and large-scale applications. This review summarizes the molecular epidemiology, evolution, and phylogeny of C. difficile, one of the most important pathogens worldwide in the current antibiotic resistance era.

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“…The tcdC gene is part of the PaLoc (encoding the toxins TcdA and TcdB and three accessory genes, tcdR, tcdE and tcdC) and encodes a putative negative regulator of TcdA and TcdB (Hundsberger et al, 1997). Truncated forms of this gene have been described previously (Spigaglia & Mastrantonio, 2002), but the presence of a deletion in the epidemic strain BI/NAP1/027 has again focused attention on the importance of such deletions and their potential role in enhanced virulence MacCannell et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Variant forms of the binary toxin CDT locus and tcdC gene in Clostridium difficile strains

Stare

Delmée

Rupnik

2007

Journal of Medical Microbiology

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Variability in the genes for toxin A, toxin B and other pathogenicity locus regions is well known and is the basis for the distribution of Clostridium difficile strains into variant toxinotypes. Previous data have indicated that some C. difficile strains have a non-functional truncated form of the binary toxin (CDT) locus. This study analysed variability in the CDT locus and the presence of deleted tcdC genes in C. difficile strains. A total of 146 strains were screened, including known variant toxinotypes and non-variant A + B + (toxinotype 0) and A " B " C. difficile strains. In all of the strains studied, only two forms of the CDT locus were found: a full-length 4.3 kb fragment encoding the functional binary toxin or a truncated 2.3 kb fragment. Whilst the full-length CDT locus was found almost exclusively in variant toxinotypes, the truncated form was detected in 79 % of toxinotype 0 strains. Non-toxinogenic A " B " strains with a truncated version were not found and only rarely possessed the full-length CDT locus (A " B " CDT + strains). Four different forms of the tcdC gene were found; three represented deleted versions and typically were found in toxinotypes III-VII, XI, XIV-XVI and XXIV. INTRODUCTIONOver the last decade, Clostridium difficile has developed into one of the most important nosocomial pathogens. This Gram-positive, sporulating micro-organism is associated with post-antibiotic intestinal infections, and the prevalence rate and disease severity seem to be rising (McDonald et al., 2006). Additionally, a new highly virulent and multiresistant type (BI/NAP1/027) has emerged recently and is spreading in Canada, the USA, the UK, the Netherlands, Belgium and France (Loo et al., 2005;Pepin et al., 2004;McDonald et al., 2005;Smith, 2005; Joseph et al., 2005;Kuijper et al., 2006;Tachon et al., 2006). In addition to high fluoroquinolone resistance, this epidemic type has some features previously known but uncommon among C. difficile isolates: variant genes for toxins A (TcdA) and B (TcdB), production of the binary toxin (CDT) and deletions in the tcdC gene.Variability in the tcdA and tcdB genes has been well studied and the strains with changed genes have been grouped into toxinotypes (Rupnik et al., 1998). Major changes are defined as deletions and RFLPs in all six PCR fragments covering tcdA and tcdB, whilst minor changes are limited to only one of the PCR fragments (usually the A3 fragment) covering the toxin genes or other pathogenicity locus (PaLoc) regions. To date, 22 toxinotypes have been described and two additional types are reported in this paper. The best-studied and the most widespread are toxinotypes III (including ribotypes 027, 034, 075 and 080) and VIII (including ribotypes 017 and 047) .Binary toxin CDT is detected in some strains in addition to TcdA and TcdB, the primary virulence factors of C. difficile (Popoff et al., 1988;Rupnik et al., 2003a). Binary toxin CDT is composed of two unlinked components, the enzymic (CDTa) and binding (CDTb) components, and acts as an actin-specific AD...

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Transcription Analysis of the Genes tcdA‐E of the Pathogenicity Locus of Clostridium Difficile

Cited by 185 publications

References 38 publications

Induction of toxins in Clostridium difficile is associated with dramatic changes of its metabolism

Induction of toxins in Clostridium difficile is associated with dramatic changes of its metabolism

Clostridium difficile infection: Evolution, phylogeny and molecular epidemiology

Variant forms of the binary toxin CDT locus and tcdC gene in Clostridium difficile strains

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