2005
DOI: 10.1086/428090
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Mechanisms by Which Anaerobic Microbiota Inhibit the Establishment in Mice of Intestinal Colonization by Vancomycin‐ResistantEnterococcus

Abstract: We used a mouse model to test the hypothesis that anaerobic microbiota in the colon inhibit the establishment of vancomycin-resistant enterococci (VRE) colonization by depleting nutrients within cecal contents and limiting the association of VRE with the mucus layer. Anaerobic growth of VRE was assessed in cecal contents and cecal mucus of mice that had received treatment with subcutaneous clindamycin or saline. VRE grew to high concentrations in cecal contents of clindamycin-treated mice and in cecal mucus of… Show more

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Cited by 59 publications
(59 citation statements)
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“…In saline treated mice, no E. faecium was detected by in situ hybridization. In contrast, the presence of E. faecium was conirmed in clindamycin-treated mice [25].…”
Section: Prevotella Clostridium Coccoides-eubacterium Rectale Clostmentioning
confidence: 89%
See 1 more Smart Citation
“…In saline treated mice, no E. faecium was detected by in situ hybridization. In contrast, the presence of E. faecium was conirmed in clindamycin-treated mice [25].…”
Section: Prevotella Clostridium Coccoides-eubacterium Rectale Clostmentioning
confidence: 89%
“…The efect of other beta lactam ATBs on the microbiota, in particular of imipenem, was also observed using the FISH method (Dubourg et al, [23] Clindamycin was used in the study dealing with development of vancomycin-resistant enterococci (VRE) because this ATB inhibits anaerobes in the intestine without the reduction of facultative Gram-negative bacilli and VRE [24]. It has been shown that clindamycin causes VRE growth in mice and colonised patients [25]. In this study, a mouse model was used to test the hypothesis that the anaerobic microlora in the large intestine inhibits development of vancomycin-resistant enterococci.…”
Section: Prevotella Clostridium Coccoides-eubacterium Rectale Clostmentioning
confidence: 99%
“…Indeed, we now know that the intestine, the most densely colonized organ in the human body, needs natural microbial colonization to maintain its structure and for normal angiogenesis, normal development of the immune system (Bager et al 2008, Ivanov et al 2008, Ivanov & Littman 2010, Negele et al 2004, Wu et al 2010), vitamin production (Backhed et al 2005, 2007, energy metabolism and homeostasis (Backhed et al 2005, Turnbaugh et al 2009), and colonization resistance (Pultz et al 2005, Wells 1990). …”
Section: General Characteristics Of the Microbiota Of Humansmentioning
confidence: 99%
“…Our attention has always been focused on the effectiveness of sanitation in restricting horizontal transmission of high-grade pathogens (Mara et al 2010), but sanitation may also limit the horizontal transmission of commensals during childhood, affecting the structure of the vertically transmitted microbiome in subsequent generations (Blaser & Falkow 2009). Despite the short-term efficiency of sanitation in reducing pathogen transmissibility (Quick et al 1996), collateral impact on the microbiome and its many roles, including its function as a shield against pathogen colonization [known as colonization resistance (Boullier et al 2003, Pultz et al 2005], has resulted.…”
Section: Modernizationmentioning
confidence: 99%
“…Antimicrobial exposures reduce the commensal gut anaerobes with compensatory increased Enterobacteriaceae and Enterococcus abundances as well as bacteriophages, allowing transmission of antibiotic resistance genes between species (4). This results in the loss of host resistance to abnormal fecal colonization and may select for MDR bacteria (5)(6)(7). Subsequently, the intestines serve as the primary reservoir of MDR bacteria (8,9).…”
mentioning
confidence: 99%