PMID- 24867962
OWN - NLM
STAT- MEDLINE
DCOM- 20150904
LR  - 20220408
IS  - 1098-6596 (Electronic)
IS  - 0066-4804 (Print)
IS  - 0066-4804 (Linking)
VI  - 58
IP  - 8
DP  - 2014 Aug
TI  - Gastrointestinal colonization with a cephalosporinase-producing bacteroides 
      species preserves colonization resistance against vancomycin-resistant 
      enterococcus and Clostridium difficile in cephalosporin-treated mice.
PG  - 4535-42
LID - 10.1128/AAC.02782-14 [doi]
AB  - Antibiotics that are excreted into the intestinal tract may disrupt the 
      indigenous intestinal microbiota and promote colonization by health 
      care-associated pathogens. beta-Lactam, or penicillin-type, antibiotics are among 
      the most widely utilized antibiotics worldwide and may also adversely affect the 
      microbiota. Many bacteria are capable, however, of producing beta-lactamase enzymes 
      that inactivate beta-lactam antibiotics. We hypothesized that prior establishment of 
      intestinal colonization with a beta-lactamase-producing anaerobe might prevent these 
      adverse effects of beta-lactam antibiotics, by inactivating the portion of 
      antibiotic that is excreted into the intestinal tract. Here, mice with a 
      previously abolished microbiota received either oral normal saline or an oral 
      cephalosporinase-producing strain of Bacteroides thetaiotaomicron for 3 days. 
      Mice then received 3 days of subcutaneous ceftriaxone, followed by either oral 
      administration of vancomycin-resistant Enterococcus (VRE) or sacrifice and 
      assessment of in vitro growth of epidemic and nonepidemic strains of Clostridium 
      difficile in murine cecal contents. Stool concentrations of VRE and ceftriaxone 
      were measured, cecal levels of C. difficile 24 h after incubation were 
      quantified, and denaturing gradient gel electrophoresis (DGGE) of microbial 16S 
      rRNA genes was performed to evaluate the antibiotic effect on the microbiota. The 
      results demonstrated that establishment of prior colonization with a 
      beta-lactamase-producing intestinal anaerobe inactivated intraintestinal ceftriaxone 
      during treatment with this antibiotic, allowed recovery of the normal microbiota 
      despite systemic ceftriaxone, and prevented overgrowth with VRE and epidemic and 
      nonepidemic strains of C. difficile in mice. These findings describe a novel 
      probiotic strategy to potentially prevent pathogen colonization in hospitalized 
      patients.
CI  - Copyright (c) 2014, American Society for Microbiology. All Rights Reserved.
FAU - Stiefel, Usha
AU  - Stiefel U
AD  - Research Service, Louis Stokes Cleveland Veterans Affairs Medical Center, 
      Cleveland, Ohio, USA Division of Infectious Diseases, Department of Medicine, 
      Case Western Reserve University, Cleveland, Ohio, USA usha.stiefel@case.edu.
FAU - Nerandzic, Michelle M
AU  - Nerandzic MM
AD  - Research Service, Louis Stokes Cleveland Veterans Affairs Medical Center, 
      Cleveland, Ohio, USA.
FAU - Pultz, Michael J
AU  - Pultz MJ
AD  - Research Service, Louis Stokes Cleveland Veterans Affairs Medical Center, 
      Cleveland, Ohio, USA.
FAU - Donskey, Curtis J
AU  - Donskey CJ
AD  - Research Service, Louis Stokes Cleveland Veterans Affairs Medical Center, 
      Cleveland, Ohio, USA Division of Infectious Diseases, Department of Medicine, 
      Case Western Reserve University, Cleveland, Ohio, USA.
LA  - eng
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20140527
PL  - United States
TA  - Antimicrob Agents Chemother
JT  - Antimicrobial agents and chemotherapy
JID - 0315061
RN  - 0 (Anti-Bacterial Agents)
RN  - 0 (RNA, Ribosomal, 16S)
RN  - 6Q205EH1VU (Vancomycin)
RN  - 75J73V1629 (Ceftriaxone)
RN  - EC 3.5.2.- (Cephalosporinase)
SB  - IM
MH  - Animals
MH  - Anti-Bacterial Agents/metabolism/*pharmacology
MH  - Bacterial Typing Techniques
MH  - Bacteroides/drug effects/*enzymology/growth & development
MH  - Ceftriaxone/metabolism/*pharmacology
MH  - Cephalosporinase/*metabolism
MH  - Clostridioides difficile/*drug effects/growth & development/pathogenicity
MH  - Colony Count, Microbial
MH  - Enterococcus/*drug effects/growth & development/pathogenicity
MH  - Feces/microbiology
MH  - Female
MH  - Gastrointestinal Tract/drug effects/microbiology
MH  - Genes, rRNA
MH  - Mice
MH  - RNA, Ribosomal, 16S/genetics
MH  - Vancomycin/pharmacology
PMC - PMC4136008
EDAT- 2014/05/29 06:00
MHDA- 2015/09/05 06:00
PMCR- 2015/02/01
CRDT- 2014/05/29 06:00
PHST- 2014/05/29 06:00 [entrez]
PHST- 2014/05/29 06:00 [pubmed]
PHST- 2015/09/05 06:00 [medline]
PHST- 2015/02/01 00:00 [pmc-release]
AID - AAC.02782-14 [pii]
AID - 02782-14 [pii]
AID - 10.1128/AAC.02782-14 [doi]
PST - ppublish
SO  - Antimicrob Agents Chemother. 2014 Aug;58(8):4535-42. doi: 10.1128/AAC.02782-14. 
      Epub 2014 May 27.