Association between production of toxins A and B and types of Clostridium difficile.

Wren, Brendan W.; Heard, S.R.; Tabaqchali, Soad

doi:10.1136/jcp.40.12.1397

Cited by 48 publications

(36 citation statements)

References 16 publications

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“…It is thus of interest to note that the same EP type has been responsible for outbreaks of infection on two continents. This is clearly an area for further study but it does lend support to the suggestions of others that there rnay be strain-specific differences in virulence [6][7][8][9] and that specific types are associated with major outbreaks [7,12,16]. In the Canadian study, more electrophoretypes (17) were found to be present in the hospital than in the Manchester group (5) and EP type 1 accounted for a lower proportion of the total isolates examined in the former.…”

Section: Discussionsupporting

confidence: 68%

“…Although these may provide the organism with much of its pathogenic potential, the spectrum and severity of clinical presentations associated with the organism may be because of variance between strains in their I12 intrinsic ability to cause disease. A number of clinical studies also support the possibility of strain-specific differences in virulence [6][7][8][9].…”

Section: Introductionmentioning

confidence: 99%

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Identification of outbreak-associated and other strains ofClostridium difficileby numerical analysis of SDS-PAGE protein patterns

et al. 1994

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SUMMARYSeventy-three cultures of Clostridium difficile isolated both during, and in the period immediately following, an outbreak of infection in a group of three hospitals, were characterized by one-dimensional sodium dodecyl sulphatepolyacrylamide gel electrophoresis (SDS-PAGE) of whole-cell proteins. Each protein pattern was characterized by the presence of one or two dense bands which were highly reproducible. The protein patterns were used as the basis for a numerical analysis which divided the strains into five phenons (electrophoretic or EP types). The majority, 60 of the 73 cultures, belonged to a single phenon which included strains from both patients and the environment. We conclude that highresolution SDS-PAGE of proteins provides an effective method for typing C. difficile and therefore for tracing the possible spread of epidemic strains in hospitals and other institutions, thereby allowing a better understanding of the epidemiology of the organism.

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Section: Discussionsupporting

confidence: 68%

Section: Introductionmentioning

confidence: 99%

Identification of outbreak-associated and other strains ofClostridium difficileby numerical analysis of SDS-PAGE protein patterns

et al. 1994

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“…This is most probably due to the amount of toxins produced (Wren et al, 1987). Some strains were reported to be deficient in TcdA production while still producing TcdB (Torres, 1991).…”

Section: Abbreviations Cddl-4 Clostridium Difficilementioning

confidence: 99%

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

Hundsberger

Braun

Weidmann

et al. 1997

European Journal of Biochemistry

184

181

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To analyse the transcription pattern of the five tcdA-E genes of the pathogenicity locus (PaLoc) of Clostridium difficile a protocol was established to purify RNA from strain VPI10463. Transcription analysis of the five tcdA-E genes showed that they were all transcribed. In the early exponential phase, a high level of tcdC and low levels of tcdA,B,D,E transcripts were detectable; this was inverted in the stationary phase, suggesting that TcdC might have a negative influence on transcription of the other genes. Three transcription initiation sites, one for tcdA and two for tcdB were determined by primer extension analysis. Readthrough transcripts from outside the locus were not obtainable, so that parts of the transcription of tcdD, tcdB, tcdA and tcdC must occur by monocistronic transcription. Within the locus all possible intergenic readthrough transcripts were detectable except that between tcdC and tcdA, a stretch of DNA interrupted by a functional transcription terminator. Thus we found mono-and polycistronic transcription of tcdA and tcdB to occur which should lead to production of a surplus of tcdA over tcdB transcripts. This would explain the surplus of TcdA over TcdB expression observed in vitro. Due to its basic nature and similarity to BcnA of Clostridium perjringens and to Orf-22 of Clostridium botulinum, TcdD is most probably a regulatory protein with DNA-binding properties. On the basis of the presented study we discuss a model for the growth-phase-related, coordinate regulation of toxin expression wherein tcdC has a negative and tcdD a positive regulatory function on transcription of the tcdD,B,E and tcdA genes.

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“…'~-'~ Some serogroups are homogeneous with regard to toxin production but others include toxigenic and non-toxigenic strains. 8 All strains of serogroup F produced cytotoxin, but toxin A production was not determined. 15 Strains from this serogroup were mainly isolated from asymptomatic infants.…”

Section: Introductionmentioning

confidence: 99%

Serogroup F strains of Clostridium difficile produce toxin B but not toxin A

Depitre¹,

Delmée

Avesani

et al. 1993

Journal of Medical Microbiology

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Summary. Most toxigenic strains of Clostridium di#iciie produce two toxins : an enterotoxin (toxin A) and a cytotoxin (toxin B). Only one strain (strain 8864) has been reported to produce toxin B but no toxin A. Serogroup F strains (44) of C. dzficile, often isolated from asymptomatic infants, have been examined for toxin production. These strains, which were from distinct geographical and clinical sources, did not produce any detectable toxin A in citro when examined in three distinct immunoassays. Nevertheless, all the strains produced a cytotoxin. Immunological differences between the cytotoxin of the serogroup F strains and that produced by C. dz3ciie strain VPI 10463 (serogroup G) were demonstrated with monoclonal antibodies specific for either the toxin B produced by C . dificiie strain VPI 10463 or C. sordellii lethal toxin (LT). Polymerase chain reaction amplification with primers derived from C. dtficile strain VPI 10463 toxin A and B genes showed that serogroup F strains seem to possess a toxin B gene homologous with that of strain VPI 10463 and at least fragments of the toxin A gene. When axenic mice were inoculated with serogroup F strains, the animals survived; they did not develop diarrhoea and no toxin A could be detected in their faeces. However, cytotoxin was detected. Furthermore, these mice were protected against subsequent challenge with the otherwise lethally toxigenic C . dzflcile strain VPI 10463. The serogroup F strains appeared to be homogeneous and distinct from other C. diflcile strains with regard to toxin production.

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Association between production of toxins A and B and types of Clostridium difficile.

Cited by 48 publications

References 16 publications

Identification of outbreak-associated and other strains ofClostridium difficileby numerical analysis of SDS-PAGE protein patterns

Identification of outbreak-associated and other strains ofClostridium difficileby numerical analysis of SDS-PAGE protein patterns

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

Serogroup F strains of Clostridium difficile produce toxin B but not toxin A

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