Prospective study of Clostridium difficile intestinal colonization and disease following single-dose antibiotic prophylaxis in surgery

Privitera, Gaetano Pierpaolo; Scarpellini, Paolo; Ortisi, G; Nicastro, Gianlucca Gonçalves; Nicolin, Roberto; Lalla, Fausto de

doi:10.1128/aac.35.1.208

Cited by 145 publications

(58 citation statements)

References 31 publications

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“…The isolation rate of 6.3% in our patients treated with ceftriaxone for 14 days was significantly lower (P < 0.0005) than that from a study by Privitera et al (12), who found C difficile in stools of 25% patients receiving ceftriaxone as a single dose for perioperative prophylaxis. The rate of isolation was also lower than expected according to our own experience.…”

contrasting

confidence: 46%

Influence of ceftriaxone on emergence of Clostridium difficile

Lejko-Zupanc

Zakelj

Strle

et al. 1992

Antimicrob Agents Chemother

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contrasting

confidence: 46%

Influence of ceftriaxone on emergence of Clostridium difficile

Lejko-Zupanc

Zakelj

Strle

et al. 1992

Antimicrob Agents Chemother

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“…Although the selection of C. difficile in fecal flora 9 and the anecdotal occurrence of CDAD following even a single dose of antibiotics are well reported, 10,11,12 prophylactic antibiotics have not been shown to be a specific risk factor for developing CDAD. 13 The large proportion of patients in both groups receiving exclusively prophylactic antibiotics (44% and 45%) reflects the frequency of surgical intervention in our hospital.…”

Section: Discussionmentioning

confidence: 99%

Risk Factors for Acquisition of Clostridium difficile–Associated Diarrhea among Outpatients at a Cancer Hospital

Palmore

Sohn

Malak

et al. 2005

Infect. Control Hosp. Epidemiol.

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Background-Clostridium difficile-associated diarrhea (CDAD) is an important infection in hospital settings. Its impact on outpatient care has not been well defined. Objective-To examine risk factors of ambulatory cancer patients with CDAD.Design-Case-control study.Setting-Memorial Sloan Kettering Cancer Center, a tertiary-care hospital.Methods-Cases of CDAD among oncology outpatients from January 1999 through December 2000 were identified via positive C. difficile toxin assay results on stool specimen sent from clinics or the emergency department. A 1:3 matched case-control study examined exposures associated with CDAD.Results-Forty-eight episodes of CDAD were identified in cancer outpatients. The median age was 51 years; 44% were female. Forty-one (85%) had received antibiotics within 60 days of diagnosis, completing courses a median of 16.5 days prior to diagnosis. Case-patients received longer courses of first-generation cephalosporins (4.8 vs 3.2 days, P = .03) and fluoroquinolones (23.6 vs 8 days; P < .01) than did control-patients. Those receiving clindamycin were 3.9-fold more likely to develop CDAD (P < .01). For each additional day of clindamycin or thirdgeneration cephalosporin exposure, patients were 1.29-and 1.26-fold more likely to develop CDAD (P < .01 and .04, respectively). The 38 CDAD patients hospitalized during the risk period (79.2%) spent more time as inpatients than control-patients (19.3 vs 9.7 days, P < .001).Conclusions-Antibiotic use, especially with cephalosporins and clindamycin, and prolonged hospitalization contributed to development of CDAD. Outpatient CDAD appears to be most strongly to be related to inpatient exposures; reasons for delayed development of symptoms are unknown.Address reprint requests to

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“…Any factor that alters the colonic flora increases the risk of C. difficile infection. Antibiotic treatment, especially broad spectrum, is the predominant risk factor for colonization that leads to C. difficile proliferation and disease (5,38). The physiological and metabolic changes in C. difficile that underlie infection during or after antibiotic stress are not known.…”

Section: Resultsmentioning

confidence: 99%

Clostridium difficile MazF Toxin Exhibits Selective, Not Global, mRNA Cleavage

et al. 2012

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e Clostridium difficile is an important, emerging nosocomial pathogen. The transition from harmless colonization to disease is typically preceded by antimicrobial therapy, which alters the balance of the intestinal flora, enabling C. difficile to proliferate in the colon. One of the most perplexing aspects of the C. difficile infectious cycle is its ability to survive antimicrobial therapy and transition from inert colonization to active infection. Toxin-antitoxin (TA) systems have been implicated in facilitating persistence after antibiotic treatment. We identified only one TA system in C. difficile strain 630 (epidemic type X), designated MazE-cd and MazF-cd, a counterpart of the well-characterized Escherichia coli MazEF TA system. This E. coli MazF toxin cleaves mRNA at ACA sequences, leading to global mRNA degradation, growth arrest, and death. Likewise, MazF-cd expression in E. coli or Clostridium perfringens resulted in growth arrest. Primer extension analysis revealed that MazF-cd cleaved RNA at the five-base consensus sequence UACAU, suggesting that the mRNAs susceptible to cleavage comprise a subset of total mRNAs. In agreement, we observed differential cleavage of several mRNAs by MazF-cd in vivo, revealing a direct correlation between the number of cleavage recognition sites within a given transcript and its susceptibility to degradation by MazF-cd. Interestingly, upon detailed statistical analyses of the C. difficile transcriptome, the major C. difficile virulence factor toxin B (TcdB) and CwpV, a cell wall protein involved in aggregation, were predicted to be significantly resistant to MazF-cd cleavage.

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Prospective study of Clostridium difficile intestinal colonization and disease following single-dose antibiotic prophylaxis in surgery

Cited by 145 publications

References 31 publications

Influence of ceftriaxone on emergence of Clostridium difficile

Influence of ceftriaxone on emergence of Clostridium difficile

Risk Factors for Acquisition of Clostridium difficile–Associated Diarrhea among Outpatients at a Cancer Hospital

Clostridium difficile MazF Toxin Exhibits Selective, Not Global, mRNA Cleavage

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