Implications for vancomycin-resistant Enterococcus colonization associated with Clostridium difficile infections

Fujitani, Shigeki; George, W. Lance; Morgan, Margie; Nichols, Stephen; Murthy, A. Rekha

doi:10.1016/j.ajic.2010.10.024

Cited by 41 publications

(25 citation statements)

References 24 publications

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“…Our results were very similar to those obtained by Garbutt et al and Rafferty et al13, 16 Similarly, Fujitani et al detected VRE colonization in 88 of the 158 C. difficile toxin positive patients 18 . VRE colonization was detected as 5.7% in toxin negatives.…”

Section: Discussionsupporting

confidence: 92%

Detection of vancomycin-resistant enterococci (VRE) in stool specimens submitted for Clostridium difficile toxin testing

Özsoy

İlki

2017

Brazilian Journal of Microbiology

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The aim of this study was to determine the association between Clostridium difficile (C. difficile) and vancomycin-resistant Enterococcus (VRE) and efficacy of screening stools submitted for C. difficile toxin assay for prevalence of VRE. Between April 2012 and February 2014, 158 stool samples submitted for C. difficile toxin to the Marmara University Microbiology Laboratory, were included in the study. Stool samples were analyzed by enzyme immuno assay test; VIDAS (bioMerieux, France) for Toxin A&B. Samples were inoculated on chromID VRE (bioMerieux, France) and incubated 24 h at 37 °C. Manuel tests and API20 STREP (bioMerieux, France) test were used to identify the Enterococci species. After the species identification, vancomycin and teicoplanin MIC's were performed by E test and molecular resistance genes for vanA vs vanB were detected by polymerase chain reaction (PCR). Of the 158 stool samples, 88 were toxin positive. The prevalence of VRE was 17%(n:19) in toxin positives however, 11.4% in toxin negatives(n:70). All VRE isolates were identified as Enterococcus faecium. These results were evaluated according to Fischer's exact chi-square test and p value between VRE colonization and C. difficile toxin positivity was detected 0.047 (p < 0.05). PPV and NPV were 79% and 47% respectively. In our study, the presence of VRE in C. difficile toxin positives is statistically significant compared with toxin negatives (p < 0.05). Screening for VRE is both additional cost and work load for the laboratories. Therefore VRE screening among C. difficile toxin positive samples, will be cost effective for determination of high risk patients in the hospitals especially for developing countries.

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Section: Discussionsupporting

confidence: 92%

Detection of vancomycin-resistant enterococci (VRE) in stool specimens submitted for Clostridium difficile toxin testing

Özsoy

İlki

2017

Brazilian Journal of Microbiology

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“…However, age-related thymic involution can result in an inability to restore immune function following infection ( 31 ). CDI effects on the thymus may influence immune function postinfection in a similar way, resulting in an increased risk of disease relapse or secondary infections, such as funguria or v ancomycin- r esistant Enterococcus (VRE) infections, which are associated with CDI patients ( 32 , 33 ). This finding is particularly relevant to elderly patients, a group at significant risk for CDI ( 34 ) who have already undergone thymic atrophy ( 31 ).…”

Section: Discussionmentioning

confidence: 99%

Defining the Roles of TcdA and TcdB in Localized Gastrointestinal Disease, Systemic Organ Damage, and the Host Response during Clostridium difficile Infections

Carter

Chakravorty

Nguyen

et al. 2015

mBio

222

212

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Clostridium difficile is a leading cause of antibiotic-associated diarrhea, a significant animal pathogen, and a worldwide public health burden. Most disease-causing strains secrete two exotoxins, TcdA and TcdB, which are considered to be the primary virulence factors. Understanding the role that these toxins play in disease is essential for the rational design of urgently needed new therapeutics. However, their relative contributions to disease remain contentious. Using three different animal models, we show that TcdA+ TcdB− mutants are attenuated in virulence in comparison to the wild-type (TcdA+ TcdB+) strain, whereas TcdA− TcdB+ mutants are fully virulent. We also show for the first time that TcdB alone is associated with both severe localized intestinal damage and systemic organ damage, suggesting that this toxin might be responsible for the onset of multiple organ dysfunction syndrome (MODS), a poorly characterized but often fatal complication of C. difficile infection (CDI). Finally, we show that TcdB is the primary factor responsible for inducing the in vivo host innate immune and inflammatory responses. Surprisingly, the animal infection model used was found to profoundly influence disease outcomes, a finding which has important ramifications for the validation of new therapeutics and future disease pathogenesis studies. Overall, our results show unequivocally that TcdB is the major virulence factor of C. difficile and provide new insights into the host response to C. difficile during infection. The results also highlight the critical nature of using appropriate and, when possible, multiple animal infection models when studying bacterial virulence mechanisms.

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“…The lack of toxicity of LPPOs when administered perorally, their stability at a wide range of pH, and their inability to be absorbed in the intestine suggest that they could be developed also into antibiotics for the treatment of GIT infections such as the commonly occurring coinfection by vancomycin-resistant Enterococcus and Clostridium difficile [ 58 ]. Applications in the prophylaxis and treatment of infections in joint surgery, where LPPO sensitive methicillin-resistant S .…”

Section: Discussionmentioning

confidence: 99%

Insights into the Mechanism of Action of Bactericidal Lipophosphonoxins

et al. 2015

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The advantages offered by established antibiotics in the treatment of infectious diseases are endangered due to the increase in the number of antibiotic-resistant bacterial strains. This leads to a need for new antibacterial compounds. Recently, we discovered a series of compounds termed lipophosphonoxins (LPPOs) that exhibit selective cytotoxicity towards Gram-positive bacteria that include pathogens and resistant strains. For further development of these compounds, it was necessary to identify the mechanism of their action and characterize their interaction with eukaryotic cells/organisms in more detail. Here, we show that at their bactericidal concentrations LPPOs localize to the plasmatic membrane in bacteria but not in eukaryotes. In an in vitro system we demonstrate that LPPOs create pores in the membrane. This provides an explanation of their action in vivo where they cause serious damage of the cellular membrane, efflux of the cytosol, and cell disintegration. Further, we show that (i) LPPOs are not genotoxic as determined by the Ames test, (ii) do not cross a monolayer of Caco-2 cells, suggesting they are unable of transepithelial transport, (iii) are well tolerated by living mice when administered orally but not peritoneally, and (iv) are stable at low pH, indicating they could survive the acidic environment in the stomach. Finally, using one of the most potent LPPOs, we attempted and failed to select resistant strains against this compound while we were able to readily select resistant strains against a known antibiotic, rifampicin. In summary, LPPOs represent a new class of compounds with a potential for development as antibacterial agents for topical applications and perhaps also for treatment of gastrointestinal infections.

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Implications for vancomycin-resistant Enterococcus colonization associated with Clostridium difficile infections

Cited by 41 publications

References 24 publications

Detection of vancomycin-resistant enterococci (VRE) in stool specimens submitted for Clostridium difficile toxin testing

Detection of vancomycin-resistant enterococci (VRE) in stool specimens submitted for Clostridium difficile toxin testing

Defining the Roles of TcdA and TcdB in Localized Gastrointestinal Disease, Systemic Organ Damage, and the Host Response during Clostridium difficile Infections

Insights into the Mechanism of Action of Bactericidal Lipophosphonoxins

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