Antimicrobial susceptibilities of Clostridium difficile.

Shuttleworth, R; Taylor, Maddison F; Jones, Daniel M.

doi:10.1136/jcp.33.10.1002

Cited by 28 publications

(19 citation statements)

References 9 publications

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“…However, only cephalosporin use also fell (figure 2A, appendix). Because all C difficile is inherently resistant to most cephalosporins, 4 their restriction cannot explain the fluoroquinolone-susceptibility-specific declines in incidence observed. Similarly, if an ST1(027)-specific factor had led to its decline, there would be no reason for C difficile infection caused by fluoroquinolone-resistant isolates of several other genotypes—ST42(106), ST3(001), and ST37(017)—in two other C difficile clades (1 and 3) 26 to decline concurrently (figure 3, figure 5).…”

Section: Discussionmentioning

confidence: 99%

“…Only toxin-positive culture-positive samples were used in the genotype-specific and phylogenetic analyses. (B) C difficile is inherently resistant to most cephalosporins 4 . IRR=annual incidence rate ratio.…”

Section: Figurementioning

confidence: 99%

“…At least three antimicrobial classes are deemed to be high-risk C difficile infection triggers, 3 including most cephalosporins, to which C difficile is inherently resistant, 4 and clindamycin, to which genotypes causing early outbreaks were resistant 5, 6, 7. Global dispersion of hypervirulent NAP1/PCR-ribotype-027 C difficile revealed an association between fluoroquinolone resistance and epidemic spread 8, 9.…”

Section: Introductionmentioning

confidence: 99%

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Effects of control interventions on Clostridium difficile infection in England: an observational study

Dingle

Didelot

Quan

et al. 2017

The Lancet Infectious Diseases

283

226

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SummaryBackgroundThe control of Clostridium difficile infections is an international clinical challenge. The incidence of C difficile in England declined by roughly 80% after 2006, following the implementation of national control policies; we tested two hypotheses to investigate their role in this decline. First, if C difficile infection declines in England were driven by reductions in use of particular antibiotics, then incidence of C difficile infections caused by resistant isolates should decline faster than that caused by susceptible isolates across multiple genotypes. Second, if C difficile infection declines were driven by improvements in hospital infection control, then transmitted (secondary) cases should decline regardless of susceptibility.MethodsRegional (Oxfordshire and Leeds, UK) and national data for the incidence of C difficile infections and antimicrobial prescribing data (1998–2014) were combined with whole genome sequences from 4045 national and international C difficile isolates. Genotype (multilocus sequence type) and fluoroquinolone susceptibility were determined from whole genome sequences. The incidence of C difficile infections caused by fluoroquinolone-resistant and fluoroquinolone-susceptible isolates was estimated with negative-binomial regression, overall and per genotype. Selection and transmission were investigated with phylogenetic analyses.FindingsNational fluoroquinolone and cephalosporin prescribing correlated highly with incidence of C difficile infections (cross-correlations >0·88), by contrast with total antibiotic prescribing (cross-correlations <0·59). Regionally, C difficile decline was driven by elimination of fluoroquinolone-resistant isolates (approximately 67% of Oxfordshire infections in September, 2006, falling to approximately 3% in February, 2013; annual incidence rate ratio 0·52, 95% CI 0·48–0·56 vs fluoroquinolone-susceptible isolates: 1·02, 0·97–1·08). C difficile infections caused by fluoroquinolone-resistant isolates declined in four distinct genotypes (p<0·01). The regions of phylogenies containing fluoroquinolone-resistant isolates were short-branched and geographically structured, consistent with selection and rapid transmission. The importance of fluoroquinolone restriction over infection control was shown by significant declines in inferred secondary (transmitted) cases caused by fluoroquinolone-resistant isolates with or without hospital contact (p<0·0001) versus no change in either group of cases caused by fluoroquinolone-susceptible isolates (p>0·2).InterpretationRestricting fluoroquinolone prescribing appears to explain the decline in incidence of C difficile infections, above other measures, in Oxfordshire and Leeds, England. Antimicrobial stewardship should be a central component of C difficile infection control programmes.FundingUK Clinical Research Collaboration (Medical Research Council, Wellcome Trust, National Institute for Health Research); NIHR Oxford Biomedical Research Centre; NIHR Health Protection Research Unit on Healthcare Associated Inf...

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Section: Discussionmentioning

confidence: 99%

Section: Figurementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Effects of control interventions on Clostridium difficile infection in England: an observational study

Dingle

Didelot

Quan

et al. 2017

The Lancet Infectious Diseases

283

226

View full text Add to dashboard Cite

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“…' 2 Recent evidence also indicates that this organism may play an aetiological role in diarrhoea' [3][4][5] and exacerbation of inflammatory bowel disease.67 Before the aetiology of PMC was delineated the unusual geographical and temporal clustering of cases implied that an infectious agent was responsible.8 '°In addition, the different carriage rates of this organism noted in infants with different types of C difficile predominating in a given centre-that is, cytotoxigenic or non-cytotoxigenic, and colonisation of infants even if delivered by caesarean section imply that the organism can be acquired from the environment'1-14 and that cross-infection may take place. Recent work has demonstrated that cross-infection probably does take place among hospitalised patients15 16 and that the organism can be isolated from the environment of patients who have been excreting C difficile.…”

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confidence: 99%

Household pets as a potential reservoir for Clostridium difficile infection.

Borriello¹,

Honour²,

Turner³

et al. 1983

J Clin Pathol

114

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SUMMARY The purpose of this study was to assess the carriage of Clostridium difficile by household pets to determine their potential as a reservoir of infection. The selective cycloserine-cefoxitin medium was used for C difficile isolation, and tissue culture used for detection of cytotoxin.Carriage of C difficile by household pets was found to be common (23%). The carriage tends to be transient and does not appear to be associated with gastrointestinal disease. Although carriage was higher in animals who had antecedent antibiotic treatment (31%) compared to those which had not (19%), the differences were not statistically significant. In most cases non-cytotoxigenic strains were isolated. Of the cytotoxigenic strains isolated at least one strain was pathogenic in a well documented animal model of human disease. Both cytotoxigenic and non-cytotoxigenic strains of C difficile could be isolated from the environment of the animals studied.

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“…Two toxins have been identified as being produced by C. difficile, namely, toxin A, an enterotoxin causing fluid accumulation in the rabbit ileal loop assay, and toxin B, a potent cytotoxin (19,22). Various studies have shown a possible correlation among the organism's resistance to antibiotics and toxin-producing capabilities and the manifestation of disease (5,29). However, apart from a few reports on the transfer of tetracycline (13,18,30) and erythromycin-clindamycin resistance (12), little is known about the molecular and genetic basis of antibiotic resistance for the organism.…”

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confidence: 99%

Molecular cloning and genetic analysis of a chloramphenicol acetyltransferase determinant from Clostridium difficile

Wren

Mullany

Clayton

et al. 1988

Antimicrob Agents Chemother

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A gene bank from a clinical isolate of Clostridium difficile expressing high chloramphenicol acetyltransferase activity was constructed by cloning Sau3A-cleaved clostridial DNA fragments into the plasmid vector pUC13. Among 1,020 clones tested, 11 were resistant to chloramphenicol; 1 of these, with an insert size of 1.9 kilobases (pPPM9), was studied further. The clone pPPM9 was mapped using a variety of restriction enzymes, and a 0.27-kilobase EcoRV-TaqI restriction fragment was shown to be within the chloramphenicol resistance (Cmr) gene by using transposon (Tn1000) mutagenesis. The 0.27-kilobase fragment and the 1.9-kilobase insert were radiolabeled and used as DNA probes in hybridization studies. Southern blot analysis with the gene probes against chromosomal DNA from Cmr strains of C. difficile obtained from five distinct geographical locations revealed that at least two copies of the same chloramphenicol acetyltransferase gene were present for each strain. Hybridization of the gene probes against Cmr strains of Staphylococcus epidermidis, Staphylococcus aureus, Klebsiella edwardsii, Escherichia coli, and to four other clostridial species revealed no homology even under conditions of low stringency.

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Antimicrobial susceptibilities of Clostridium difficile.

Cited by 28 publications

References 9 publications

Effects of control interventions on Clostridium difficile infection in England: an observational study

Effects of control interventions on Clostridium difficile infection in England: an observational study

Household pets as a potential reservoir for Clostridium difficile infection.

Molecular cloning and genetic analysis of a chloramphenicol acetyltransferase determinant from Clostridium difficile

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