scholarly journals Efficacy of Probiotic for Inhibition of Intestinal Colonization by Vancomycin-resistant Enterococci

2008 ◽  
Vol 12 ◽  
pp. e211-e212
Author(s):  
H. Fazeli ◽  
B. Nasr Esfahani ◽  
M. Mirlohi
2008 ◽  
Vol 74 (7) ◽  
pp. 1997-2003 ◽  
Author(s):  
Mathieu Millette ◽  
Gilbert Cornut ◽  
Claude Dupont ◽  
François Shareck ◽  
Denis Archambault ◽  
...  

ABSTRACT This study demonstrated the capacity of bacteriocin-producing lactic acid bacteria (LAB) to reduce intestinal colonization by vancomycin-resistant enterococci (VRE) in a mouse model. Lactococcus lactis MM19 and Pediococcus acidilactici MM33 are bacteriocin producers isolated from human feces. The bacteriocin secreted by P. acidilactici is identical to pediocin PA-1/AcH, while PCR analysis demonstrated that L. lactis harbors the nisin Z gene. LAB were acid and bile tolerant when assayed under simulated gastrointestinal conditions. A well diffusion assay using supernatants from LAB demonstrated strong activity against a clinical isolate of VRE. A first in vivo study was done using C57BL/6 mice that received daily intragastric doses of L. lactis MM19, P. acidilactici MM33, P. acidilactici MM33A (a pediocin mutant that had lost its ability to produce pediocin), or phosphate-buffered saline (PBS) for 18 days. This study showed that L. lactis and P. acidilactici MM33A increased the concentrations of total LAB and anaerobes while P. acidilactici MM33 decreased the Enterobacteriaceae populations. A second in vivo study was done using VRE-colonized mice that received the same inocula as those in the previous study for 16 days. In L. lactis-fed mice, fecal VRE levels 1.73 and 2.50 log10 CFU/g lower than those in the PBS group were observed at 1 and 3 days postinfection. In the P. acidilactici MM33-fed mice, no reduction was observed at 1 day postinfection but a reduction of 1.85 log10 CFU/g was measured at 3 days postinfection. Levels of VRE in both groups of mice treated with bacteriocin-producing LAB were undetectable at 6 days postinfection. No significant difference in mice fed the pediocin-negative strain compared to the control group was observed. This is the first demonstration that human L. lactis and P. acidilactici nisin- and pediocin-producing strains can reduce VRE intestinal colonization.


2005 ◽  
Vol 49 (8) ◽  
pp. 3513-3516 ◽  
Author(s):  
Nicole J. Pultz ◽  
Usha Stiefel ◽  
Curtis J. Donskey

ABSTRACT In mice, vancomycin and linezolid treatment disrupted the anaerobic intestinal microflora, based on denaturing gradient gel electrophoresis analysis, and promoted colonization by Klebsiella pneumoniae and vancomycin-resistant enterococci. However, the effects varied depending on dose and duration of treatment. Daptomycin treatment did not disrupt the anaerobic microflora or promote either pathogen.


2006 ◽  
Vol 50 (2) ◽  
pp. 596-599 ◽  
Author(s):  
Camilla H. Lester ◽  
Niels Frimodt-Møller ◽  
Thomas Lund Sørensen ◽  
Dominique L. Monnet ◽  
Anette M. Hammerum

ABSTRACT Transient colonization by vancomycin-resistant enterococci of animal origin has been documented in the intestines of humans. However, little is known about whether transfer of the vanA gene occurs in the human intestine. Six volunteers ingested a vancomycin-resistant Enterococcus faecium isolate of chicken origin, together with a vancomycin-susceptible E. faecium recipient of human origin. Transconjugants were recovered in three of six volunteers. In one volunteer, not only was vancomycin resistance transferred, but also quinupristin-dalfopristin resistance. This study shows that transfer of the vanA gene from an E. faecium isolate of animal origin to an E. faecium isolate of human origin can occur in the intestines of humans. It suggests that transient intestinal colonization by enterococci carrying mobile elements with resistance genes represents a risk for spread of resistance genes to other enterococci that are part of the human indigenous flora, which can be responsible for infections in certain groups of patients, e.g., immunocompromised patients.


2015 ◽  
Vol 148 (4) ◽  
pp. S-724-S-725
Author(s):  
Abhishek Deshpande ◽  
Kelly Hurless ◽  
Jennifer L. Cadnum ◽  
Laurent Chesnel ◽  
Luisa Chan ◽  
...  

2004 ◽  
Vol 48 (6) ◽  
pp. 2144-2148 ◽  
Author(s):  
Usha Stiefel ◽  
Nicole J. Pultz ◽  
Marion S. Helfand ◽  
Curtis J. Donskey

ABSTRACT Ramoplanin is a glycolipodepsipeptide antibiotic with activity against gram-positive bacteria that is in clinical trials for prevention of vancomycin-resistant Enterococcus (VRE) bloodstream infections and treatment of Clostridium difficile diarrhea. Orally administered ramoplanin suppresses VRE intestinal colonization, but recurrences after discontinuation of treatment have frequently been observed. We used a mouse model to examine the efficacy of ramoplanin for inhibition of VRE colonization and evaluated the etiology of recurrences of colonization. Eight days of treatment with ramoplanin (100 μg/ml) in drinking water suppressed VRE to undetectable levels, but 100% of mice developed recurrent colonization; a higher dose of 500 μg/ml in water was associated with recurrent colonization in 50% of mice. Two of eight (25%) mice treated with the 100-μg/ml dose of ramoplanin had low levels of VRE in their cecal tissues on day 8 despite undetectable levels in stool and cecal contents. Mice that received prior ramoplanin treatment did not develop VRE overgrowth when challenged with 107 CFU of oral VRE 1, 2, or 4 days later. In communal cages, rapid cross-transmission and overgrowth of VRE was observed among clindamycin-treated mice; ramoplanin treatment effectively suppressed VRE overgrowth in such communal cages. Ramoplanin treatment promoted increased density of indigenous Enterobacteriaceae and overgrowth of an exogenously administered Klebsiella pneumoniae isolate. These results demonstrate the efficacy of ramoplanin for inhibition of VRE colonization and suggest that some recurrences occur due to reexpansion of organisms that persist within the lining of the colon. Ramoplanin treatment may be associated with overgrowth of gram-negative bacilli.


2015 ◽  
Vol 60 (1) ◽  
pp. 628-631 ◽  
Author(s):  
Peter Seiler ◽  
Michel Enderlin-Paput ◽  
Philippe Pfaff ◽  
Maria Weiss ◽  
Daniel Ritz ◽  
...  

ABSTRACTThe promotion of colonization with vancomycin-resistant enterococci (VRE) is one potential side effect during treatment ofClostridium difficile-associated diarrhea (CDAD), resulting from disturbances in gut microbiota. Cadazolid (CDZ) is an investigational antibiotic with potentin vitroactivity againstC. difficileand against VRE and is currently in clinical development for the treatment of CDAD. We report that CDZ treatment did not lead to intestinal VRE overgrowth in mice.


2010 ◽  
Vol 48 (7) ◽  
pp. 2595-2598 ◽  
Author(s):  
M. Vidal ◽  
C. Forestier ◽  
N. Charbonnel ◽  
S. Henard ◽  
C. Rabaud ◽  
...  

2006 ◽  
Vol 27 (10) ◽  
pp. 1076-1080 ◽  
Author(s):  
Ji Young Huh ◽  
Wee Gyo Lee ◽  
Hye Young Jin

Objective:To compare the molecular characteristics of infection-derived (ID) isolates and intestinal colonization–derived (ICD) isolates of vancomycin-resistant enterococci (VRE) recovered from hospitalized patients.Design.A 12-month prospective cohort study.Setting.A 1,000-bed teaching facility.Methods.From January through December 2004, a total of 30 pairs ofvanA-containing enterococcal isolates were collected from patients admitted to a teaching hospital in South Korea. Each pair comprised an ID and an ICD VRE isolate from the same patient. All VRE isolates were investigated on the basis ofSmaI-restricted pulsed-field gel electrophoresis (PFGE) pattern, Tn1546type, and presence of theespgene, including A and C repeat number variation.Results.Members of 19 pairs (63%) of VRE isolates were genetically indistinguishable from each other. The 11 patients for whom the molecular characteristics of the ID isolates differed from those of the ICD isolates had longer durations of hospitalization and intensive care unit (ICU) stay, compared with the other 19 patients.Conclusions.These findings suggest the longer durations of hospitalization and ICU stay may be possible risk factors for colonization with multiple clones of VRE.


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