Vancomycin-resistant Enterococci Colonization Research Articles

Decrease in vancomycin-resistant Enterococcus colonization associated with a reduction in carbapenem use as empiric therapy for febrile neutropenia in patients with acute leukemia.

To compare the effects of empiric carbapenems versus cycling cefepime and piperacillin/tazobactam on the rates of vancomycin-resistant Enterococcus (VRE) colonization, bloodstream infections, and outcomes of patients admitted with acute leukemia. Retrospective clinical study with VRE molecular strain typing and gastrointestinal microbiome comparison. A regional referral center for acute leukemia. 342 consecutive patients admitted with newly diagnosed acute leukemia. In September 2015, we changed our empiric antibiotic of choice for neutropenic fever from a carbapenem to the cycling regimen. We studied 214 consecutive patients during the carbapenem period and 128 during the cycling period. Surveillance for VRE stool colonization was conducted weekly. Representative stool samples were analyzed for VRE MLST types and changes in the composition and diversity of the fecal microbiota. The change in empiric antibiotics was associated with a significant decrease in VRE colonization (hazard ratio [HR], 0.35; 95% confidence interval [CI], 0.27-0.66), a switch in the dominant VRE MLST types on the unit, and some modifications in the gastrointestinal microbiome. There were no differences in total gram-positive or gram-negative BSIs. During the carbapenem period, we observed higher absolute numbers of Candida spp and fewer ESBL BSIs, but these did not reach statistical significance. Patients during the carbapenem period had longer lengths of stay and durations of severe neutropenia and 10% higher hospital cost. Carbapenem-sparing empiric antibiotic regimens may have advantages related to VRE ecology, gastrointestinal dysbiosis, duration of neutropenia, cost and length of stay.

Vancomycin-resistant Enterococcus (VRE) outbreak in a neonatal intensive care unit and special care nursery at a tertiary-care hospital in Australia-A retrospective case-control study.

We investigated the risk factors and origins of the first known occurrence of VRE colonization in the neonatal intensive care unit (NICU) at the Canberra Hospital. A retrospective case-control study. A 21-bed neonatal intensive care unit (NICU) and a 15-bed special care nursey (SCN) in a tertiary-care adult and pediatric hospital in Australia. All patients admitted to the NICU and SCN over the outbreak period: January-May 2017. Of these, 14 were colonized with vancomycin-resistant Enterococcus (VRE) and 77 were noncolonized. Demographic and clinical variables of cases and controls were compared to evaluate potential risk factors for VRE colonization. Whole-genome sequencing of the VRE isolates was used to determine the origin of the outbreak strain. Swift implementation of wide-ranging infection control measures brought the outbreak under control. Multivariate logistic regression revealed a strong association between early gestational age and VRE colonization (odds ratio [OR], 3.68; 95% confidence interval [CI], 1.94-7.00). Whole-genome sequencing showed the isolates to be highly clonal Enterococcus faecium ST1421 harboring a vanA gene and to be closely related to other ST1421 previously sequenced from the Canberra Hospital and the Australian Capital Territory. The colonization of NICU patients was with a highly successful clone endemic to the Canberra Hospital likely introduced into the NICU environment from other wards, with subsequent cross-contamination spreading among the neonate patients. Use of routine surveillance screening may have identified colonization at an earlier stage and have now been implemented on a 6-monthly schedule.

Risk Factors and Outcomes of Vancomycin-Resistant Versus Vancomycin-Sensitive Enterococcal Bloodstream Infections in Patients With Acute Myeloid Leukemia

Background Studies have shown increased mortality from vancomycin-resistant enterococcal (VRE) bloodstream infections (BSI) in neutropenic patients. Whether these mortality differences pertain to acute myeloid leukemia (AML) patients is unknown. We compared risk factors and outcomes between VRE and vancomycin-sensitive enterococcal (VSE) BSIs in AML patients. Methods We conducted a single-center, 5-year, retrospective cohort study of AML patients with enterococcal BSI. Neutropenia duration, Enterococcus species, vancomycin exposure, VRE colonization, 7- and 30-day mortality, age, sex, length of stay, and central line status were compared and analyzed. Results There were a total of 77 AML patients with enterococcal BSI, 54.5% had VRE. Enterococcus faecalis and Enterococcus faecium accounted for 28.5% and 62.3% of BSI, respectively. The E. faecalis isolates were more likely to be VSE (91% vs 9%, P < 0.001) and E. faecium isolates to be VRE (71% vs 29%, P < 0.001). Duration of neutropenia was significantly longer (27.3 days vs 2.7 days, P < 0.005) among VRE patients. Recent vancomycin use and VRE colonization were associated with VRE BSI. There were no differences in bacteremia duration, length of stay, or 7- and 30-day mortality between VRE and VSE BSI. Conclusion Enterococcal infections among AML patients are more likely to be caused by vancomycin-resistant E. faecium. The risk is increased by VRE colonization and vancomycin exposure. In a relatively homogenous group of patients, treatment-related factors may affect outcome more than species type or susceptibility of bacterial isolates. This finding is important for future development of patient education, preventive, and treatment protocols.

A retrospective cohort study of antibiotic exposure and vancomycin-resistant Enterococcus recolonization.

In the National Institutes of Health (NIH) Clinical Center, patients colonized or infected with vancomycin-resistant Enterococcus (VRE) are placed in contact isolation until they are deemed "decolonized," defined as having 3 consecutive perirectal swabs negative for VRE. Some decolonized patients later develop recurrent growth of VRE from surveillance or clinical cultures (ie, "recolonized"), although that finding may represent recrudescence or new acquisition of VRE. We describe the dynamics of VRE colonization and infection and their relationship to receipt of antibiotics. In this retrospective cohort study of patients at the National Institutes of Health Clinical Center, baseline characteristics were collected via chart review. Antibiotic exposure and hospital days were calculated as proportions of VRE decolonized days. Using survival analysis, we assessed the relationship between antibiotic exposure and time to VRE recolonization in a subcohort analysis of 72 decolonized patients. In total, 350 patients were either colonized or infected with VRE. Among polymerase chain reaction (PCR)-positive, culture (Cx)-negative (PCR+/Cx-) patients, PCR had a 39% positive predictive value for colonization. Colonization with VRE was significantly associated with VRE infection. Among 72 patients who met decolonization criteria, 21 (29%) subsequently became recolonized. VRE recolonization was 4.3 (P = .001) and 2.0 (P = .22) times higher in patients with proportions of antibiotic days and antianaerobic antibiotic days above the median, respectively. Colonization is associated with clinical VRE infection and increased mortality. Despite negative perirectal cultures, re-exposure to antibiotics increases the risk of VRE recolonization.

Two Strains of Lactobacilli Effectively Decrease the Colonization of VRE in a Mouse Model.

Vancomycin-resistant Enterococcus (VRE) infection is a serious challenge for clinical management and there is no effective treatment at present. Fecal microbiota transplantation (FMT) and probiotic intervention have been shown to be promising approaches for reducing the colonization of certain pathogenic bacteria in the gastrointestinal tract, however, no such studies have been done on VRE. In this study, we evaluated the effect of FMT and two Lactobacillus strains (Y74 and HT121) on the colonization of VRE in a VRE-infection mouse model. We found that both Lactobacilli strains reduced VRE colonization rapidly. Fecal microbiota and colon mRNA expression analyses further showed that mice in FMT and the two Lactobacilli treatment groups restored their intestinal microbiota diversity faster than those in the phosphate buffer saline (PBS) treated group. Administration of Lactobacilli restored Firmicutes more quickly to the normal level, compared to FMT or PBS treatment, but restored Bacteroides to their normal level less quickly than FMT did. Furthermore, these treatments also had an impact on the relative abundance of intestinal microbiota composition from phylum to species level. RNA-seq showed that FMT treatment induced the expression of more genes in the colon, compared to the Lactobacilli treatment. Defense-related genes such as defensin α, Apoa1, and RegIII were down-regulated in both FMT and the two Lactobacilli treatment groups. Taken together, our findings indicate that both FMT and Lactobacilli treatments were effective in decreasing the colonization of VRE in the gut.

Vancomycin use in surrounding patients during critical illness and risk for persistent colonization with vancomycin-resistant Enterococcus

The optimal duration of contact precautions for vancomycin-resistant enterococcus (VRE)-colonized patients is uncertain and individual patient characteristics alone may not predict risk of prolonged colonization. Using a cohort of adult patients who underwent testing for VRE at intensive care unit (ICU) admission, we tested the association between local (unit-level) vancomycin use and persistent colonization with VRE. Higher unit-level vancomycin use significantly prolonged VRE colonization (P=0.03) independent of patient-level vancomycin use and unit VRE density.

Genetic typing of Enterococcus faecium VRE strains isolated in three hospitals in Warsaw and Siedlce in 2015-2016

Since the first report of vancomycin-resistant enterococci (VRE) in Poland, in 1996, these strains have spread in Polish hospitals, mainly due to selective pressure associated with increased use of vancomycin in the treatment of infections caused by methicillin-resistant staphylococci and Clostridium difficile. At the beginning of 2016 a growing number of patients colonized with VRE in the gastrointestinal tract was observed in the Children’s Memorial Health Institute (IPCZD). Some of these patients were transferred from other hospitals, and VRE colonization was found on admission. To analyze genetic similarity of VRE strains isolated from patients hospitalized in IPCZD and two other hospitals in Mazovian district, genetic typing by pulsed field gel electrophoresis (PFGE) was performed. VRE strains were isolated from rectal swabs, and other clinical samples such as blood, cerebrospinal fluid, other body fluids, and environmental samples. A total of 56 VRE strains from IPCZD, 20 strains from Siedlce and 4 strains from patients from Grochowski Hospital in Warsaw were typed by PFGE. PFGE typing revealed 4 VRE clones containing several strains with identical restriction patterns. Among VRE strains isolated from neonates hospitalized in IPCZD, two clones with 24 and 20 identical strains were found. Respectively, 16 (67%) and 12 (60%) isolates were originated from rectal swabs from patients at admission to the hospital. Clonal strains were identified in all three hospitals included in the study. Our results showed that VRE strains had spread in the region. Isolation of clonal strains on admission to the hospital suggested independent VRE introductions from environment or other hospitals. Identification of clonal strains obtained from rectal swabs and other clinical samples during hospitalization indicated horizontal transmission.

Incidence of Vancomycin Resistant Enterococci Colonization in Zagazig University Pediatric ICU

Incidence of Vancomycin Resistant Enterococci Colonization in Zagazig University Pediatric ICU

Magnitude of Vancomycin-Resistant Enterococci (VRE) Colonization among HIV-Infected Patients Attending ART Clinic in West Amhara Government Hospitals.

Background Enterococci that colonize the intestinal tract of immunocompromised patients are an important cause of nosocomial infections. Data on the prevalence of vancomycin-resistant Enterococci (VRE) and its antimicrobial susceptibility patterns and associated factors are scarce in the present study area. Therefore, this study was conducted aimed at determining the prevalence of VRE colonization among HIV-infected patients attending ART clinic at West Amhara Government Hospitals. Methods A cross-sectional study was conducted from 1 February 2017 to 31 May 2017. A total of 349 HIV patients were included in the study. A pretested structured questionnaire was used to collect sociodemographic data and possible associated factors for VRE colonization. Identification and confirmation of Enterococci from stool sample was performed based on the standard procedures. Antimicrobial susceptibility testing was done using the Kirby–Bauer disk diffusion method on the Muller–Hinton agar plate as per the standard protocol, and resistance profile of the isolates was determined according to Clinical and Laboratory Standards Institute (CLIS). Data were analyzed using SPSS v23. Descriptive analysis was used to visualize differences within data. Moreover, the stepwise logistic regression model was done to assess factors associated with VRE colonization. P value was set at 0.05 to indicate statistical significance difference. Results The overall colonization status of Enterococci was at 63% (220/349). The VRE colonization was at 17 (7.7% (95% CI: 4.9–12.0)). Among Enterococcal isolates tested for antimicrobial susceptibility, 142 (64.5%) were found resistant to two or more antibiotics. Antibiotic treatment (for >2 weeks) and history of hospital admission in the last six month were found statistically associated for VRE colonization (AOR = 10.18, (95% CI: 1.9–53.20)) and (AOR = 20.17; (95% CI: 5.22–77.93)), respectively. Conclusions The observed VRE with multidrug resistance colonization need a periodic surveillance of antimicrobial testing to detect emerging resistance and prevent the spread of further drug resistance.

Vancomycin resistant enterococcal (VRE) colonization among patients treated in intensive care units at the National Hospital of Sri Lanka, and determination of genotype/s responsible for resistance

The aim of this study was to assess the epidemiology of VRE colonization among patients in the intensive care units (ICU) of the National Hospital of Sri Lanka (NHSL). A cross sectional study was carried out on 218 patients admitted to 12 ICUs of the NHSL from January to March 2012. Rectal swabs were collected on day 0, 4, 8 and every 4th day thereafter till discharge. Enterococci were isolated on selective media and identified up to species level using standard bacteriological procedures. Standardized disc diffusion antibiotic susceptibility testing to ampicillin, teicoplanin and vancomycin was performed using the Clinical and Laboratory Standards Institute (CLSI) method. Minimum inhibitory concentrations to vancomycin were determined, using the E-test in strains showing intermediate or frank resistance to vancomycin by disc diffusion. Genotype determination (van A / van B) was carried out on isolates identified as VRE using the polymerase chain reaction. Patients positive for VRE colonization were followed up to discharge or death. VRE prevalence in the study sample was 5%. Univariate analysis showed that the use of metronidazole (odds ratio [OR] :15.73;95% 95% confidence interval [CI] : 3.94-62.67,P<0.05) or teicoplanin (OR: 12.56; 95% CI:2.65 – 59.52, p< 0.05) and diabetes (OR: 05.13; 95% CI: 1.36 – 18.7, p< 0.05) or hemodialysis during ICU stay (OR: 7.38 ;95% CI : 1.69-32.16, P<0.05) were associated with an increased risk of VRE colonization. The 5% prevalence of VRE colonization detected signals the emergence of VRE in the intensive care setting in Sri Lanka.

Fecal microbiota transplantation to eradicate vancomycin-resistant enterococci colonization in case of an outbreak

ObjectiveA rapid and worrying emergence of vancomycin-resistant enterococci (VRE) gut colonization is occurring worldwide and may be responsible for outbreaks, especially in healthcare facilities. While no efficient decolonization strategies are recommended, we assessed fecal microbiota transplantation (FMT) to eradicate VRE colonization. Patients and methodOur main objective was to measure the impact of FMT on decolonization of VRE carriers, confirmed by at least two consecutive negative rectal swabs at one-week interval during a 3-month follow-up period. Patients received no antibiotic prior to the FMT. ResultsAfter a month only three patients remained colonized with VRE. Decolonization was associated with 87.5% (n=7) of success after three months as only one patient remained colonized. ConclusionOur first results confirm that the FMT seems to be safe, with an impact on VRE colonization over time that may help control outbreaks.

Impact of Empiric Treatment for Vancomycin-Resistant Enterococcus in Colonized Patients Early after Allogeneic Hematopoietic Stem Cell Transplantation

In recent years, vancomycin-resistant Enterococcus (VRE) colonization is being increasingly encountered in transplant recipients, and VRE has become one of the leading causes of bacteremia early after allogeneic hematopoietic stem cell transplantation (allo-HSCT). Data are sparse on the effect of empiric VRE therapy for febrile, neutropenic allo-HSCT recipients colonized with VRE. All allo-HSCT recipients aged ≥18years who developed VRE bacteremia (VREB) between 2005 and 2014 were identified and categorized as to whether they received empiric or directed VRE therapy. There were 434 (33%) VRE-colonized and 872 (67%) non-VRE-colonized patients during the study period, and 172 of the 434 (40%) VRE-colonized patients received empiric therapy. There was no significant difference in incidence of VREB among colonized patients who did or did not receive empiric therapy (28 of 172 [16%] vs 55 of 262 [21%]; P = .22). There were 95 patients with VREB, of which the majority (83 of 95; 87%) was known to be VRE-colonized. Of the 95 VREB episodes, 29 (31%) were treated with empiric VRE therapy, whereas 66 (69%) were treated with directed therapy. No significant differences in clinical outcomes, including median duration of bacteremia (2 days vs 2 days; P = .39), recurrent VREB (3 of 29 [10%] vs 5 of 66 [8%]; P = .65), 30-day all-cause mortality (1 of 29 [3%] vs 4 of 66 [6%]; P = .62), or VRE-attributable mortality (1 of 29 [3%] vs 1 of 66 [2%]; P = .55), were observed between the empiric therapy and directed therapy groups. Kaplan-Meier curve analysis showed no significant difference in survival at 30days in allo-HSCT recipients with VREB who received empiric therapy and those who received directed therapy (97% vs 94%; P = .62). Based on our data, we recommend against empiric use of VRE-active agents for fever and neutropenia in VRE-colonized patients undergoing allo-HSCT.

A Case Report of a Stroke Patient with Vancomycin-Resistant Enterococci Colonization Treated with Korean Medicine, Especially &lt;italic&gt;Gami-sipjeondaebo-tang&lt;/italic&gt;

Objectives We treated a stroke patient with vancomycin-resistant enterococci (VRE) colonization using Gami-sipjeondaebo-tang. Methods A patient diagnosed with intracranial hemorrhage with VRE colonization was treated with herbal medicine and acupuncture. We checked general conditions every day and performed stool VRE culture once a week. We evaluated the improvement of symptoms by change in VAS grade, general weakness, and stool VRE culture results. Results After a treatment of Gami-sipjeondaebo-tang combined with acupuncture therapy, improvement of the general condition was observed. Also, VRE colonization was no longer detected in the stool culture. Conclusions This case report proved the effect of Korean medicine for a stroke patient with VRE colonization, but further study is needed. Keywords: vancomycin resistant enterococci, Korean medicine, Gami-sipjeondaebo-tang, case report

Gastric Acid Suppression May Lead to an Increased Risk of Vancomycin-Resistant Enterococcus Colonization: Presidential Poster Award

Introduction: Gastric acid suppression therapy has been reported to change the gastrointestinal microbiome, resulting in increased gastrointestinal infections. However, the effect of gastric acid suppression therapy on vancomycin-resistant enterococcus (VRE) colonization has not been investigated. Methods: Subjects who had surveillance rectal swabs for VRE at a university hospital were investigated. Surveillance was performed on subjects with prior hospitalization within 3months, history of VRE colonization/infection, or positive VRE findings from an adjacent patient. Gastric acid suppression therapy was defined as use of proton pump inhibitor or histamine-receptor-2 antagonists. Results: Of 886 subjects who underwent VRE screening, 452 were included with 69 VRE positive and 383 VRE negative subjects. In univariable analysis, gastric acid suppression therapy, antibiotics use, male gender and prior hospitalization were significant risk factors for VRE colonization. Multivariable analysis showed that gastric acid suppression therapy (OR 2.873, 95% CI 1.473-5.605, P=0.002) and antibiotics use (OR 3.896, 95% CI 2.019-7.520, P<0.001) significantly increased VRE risk. Of antibiotics, carbapenems (OR 3.836, 95% CI 1.603-9.182, P=0.003) glycopeptides (OR 2.784, 95% CI 1.155-6.712, P=0.023), and cephalosporins (OR 2.210, 95% CI 1.213-4.025, P=0.010) were most significantly associated with VRE colonization. The unfavorable effect of gastric acid suppression therapy on VRE colonization was consistent, regardless of antibiotics type. Conclusion: Gastric acid suppression therapy significantly increased VRE colonization risk. Gastric acid suppression should be administered according to strict guidelines. Physicians should be made aware of the increased VRE risk, and should consider VRE surveillance in those under long-term gastric suppression therapy.1112_A Figure 1. Characteristics of the study subjects1112_B Figure 2. Antibiotics use in the study subjects1112_C Figure 3. Multivariable analysis of VRE risk factors

Practical methods for effective vancomycin-resistant enterococci (VRE) surveillance: experience in a liver transplant surgical intensive care unit.

We evaluated the utility of vancomycin-resistant Enterococcus (VRE) surveillance by varying 2 parameters: admission versus weekly surveillance and perirectal swabbing versus stool sampling. Prospective, patient-level surveillance program of incident VRE colonization. Liver transplant surgical intensive care unit (SICU) of a tertiary-care referral medical center with a high prevalence of VRE.PatientsAll patients admitted to the SICU from June to August 2015. We conducted a point-prevalence estimate followed by admission and weekly surveillance by perirectal swabbing and/or stool sampling. Incident colonization was defined as a negative screen followed by positive surveillance. VRE was detected by culture on Remel Spectra VRE chromogenic agar. Microbiologically-confirmed VRE bloodstream infections (BSIs) were tracked for 2 months. Statistical analyses were calculated using the McNemar test, the Fisher exact test, the t test, and the χ2 test. In total, 91 patients underwent VRE surveillance testing. The point prevalence of VRE colonization was 60.9%; VRE prevalence on admission was 30.1%. Weekly surveillance identified an additional 7 of 28 patients (25.0%) with incident colonization. VRE BSIs were more common in VRE-colonized patients than in noncolonized patients (8 of 43 vs 2 of 48; P=.028). In a direct comparison, perirectal swabs were more sensitive than stool samples in detecting VRE (64 of 67 vs 56 of 67; P=.023). Compliance with perirectal swabbing was 89% (201 of 226) compared to 56% (127 of 226) for stool collection (P≤0.001). We recommend weekly VRE surveillance over admission-only screening in high-burden units such as liver transplant SICUs. Perirectal swabs had greater collection compliance and sensitivity than stool samples, making them the preferred methodology. Further work may have implications for antimicrobial stewardship and infection control.

Chlorhexidine-based body washing for colonization and infection of methicillin-resistant &lt;em&gt;Staphylococcus aureus&lt;/em&gt; and vancomycin-resistant &lt;em&gt;Enterococcus&lt;/em&gt;: an updated meta-analysis

BackgroundThe effects of chlorhexidine-based body washing (CHW) on health care-associated infections have been reported in numerous studies, while their findings remain conflicting. This study aims to update the evidence for the effects of CHW on the risk of colonization or infection with hospital-acquired methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant Enterococcus (VRE).MethodsTwo independent authors searched PubMed, Embase, and Cochrane Library from inception through February 2018. We selected all observational studies or clinical trials for the effect of CHW on the risk of colonization and infection with hospital-acquired MRSA or VRE. Random-effects models were applied to calculate summary incidence rate ratios (IRRs) for the related associations.ResultsOf 140 records identified, we obtained data from 17 relevant articles for meta-analysis. Compared with patients without antiseptic bathing, patients with CHW had a significantly lower risk of MRSA colonization (IRR 0.61, 95% CI 0.48–0.77) and VRE colonization (IRR 0.58, 95% CI 0.42–0.80). Similarly, we also noted that patients with CHW had a significantly lower risk of MRSA infection (IRR 0.65, 95% CI 0.52–0.81). However, no significantly lower risk of VRE infection (IRR 0.61, 95% CI 0.30–1.25) was noted in patients with CHW. Sensitivity analyses or trim-and-fill method confirmed the robustness of the findings.ConclusionCurrent evidence supports that patients with CHW had a significantly lower risk of MRSA or VRE colonization and a lower risk of MRSA infection. More evidence should be accumulated to reinforce these findings, especially on the effect of CHW on the risk of VRE infection.

Engineered E. coli Nissle 1917 for the reduction of vancomycin-resistant Enterococcus in the intestinal tract.

Vancomycin‐resistant Enterococcus (VRE) poses a serious threat in hospitals where they densely colonize the intestinal tracts of patients. In vulnerable hosts, these pathogens may translocate to the bloodstream and become lethal. The ability to selectively reduce VRE in the intestinal tracts of patients could potentially prevent many of these translocation events and reduce the spread of the pathogen. Herein, we have engineered Escherichia. coli Nissle 1917 to produce and secrete three antimicrobial peptides, Enterocin A, Enterocin B, and Hiracin JM79, to specifically target and kill Enterococcus. These peptides exhibited potent activity against both Enterococcus faecium and Enterococcus faecalis, the two most prominent species responsible for VRE infections. We first discuss the optimization of the system used to express and secrete the peptides. We then show that by simultaneously expressing these peptides, both E. faecium and E. faecalis were drastically inhibited. We then demonstrate a suppression of the development of resistance when supernatant from the E. coli producer strains was used to treat E. faecium. Finally, we tested the efficacy of the probiotic in a VRE colonization model in mice. These studies showed that administration of the engineered probiotic significantly reduced the levels of both E. faecium and E. faecalis in the feces of male Balb/cJ mice.

Similarities and Differences in Risk Factors for Vancomycin-resistant Enterococcus Colonization between an Acute Hospital and its affiliated Intermediate- and Long-term care facilities

Background: Vancomycin-resistant Enterococci (VRE) infections in acute hospitals (AHs) are increasing, but little is known in intermediate- and long-term care facilities (ILTCs). Patients often transfer between AHs and ILTCs. We sought to compare risk factors for VRE colonization between an AH and ILTCs in a healthcare network. Methods & Materials: Two cross-sectional studies were conducted in a 1600-bed tertiary-care AH and its six affiliated ILTCs in June-July 2014 and June-July 2015. Rectal swabs or stool were cultured for VRE. Clinical data were obtained from medical records and associations with colonization made. To control for confounding, multivariable logistic regression models were constructed. Results: Of 3469 patients screened, 11.4% were colonized with VRE. VRE prevalence was higher in the AH(16.9%) than ILTCs(4.4%)(OR 2.75, 95%CI 1.96-3.86, P < 0.001). After adjusting for age, gender, screening year, and co-morbidities, risk factors for VRE colonization in the AH included length of stay(LOS) >14 days(OR 1.67, 95%CI 1.27-2.21, P < 0.001), number of beds in hospital room(OR 1.08 95%CI 1.02-1.15, P = 0.009), presence of wounds(OR 1.82 95%CI 1.39-2.39, P < 0.001), as well as prior admission to the AH(OR 1.42, 95%CI 1.07-1.88, P = 0.014), prior VRE carriage(OR 4.92 95%CI 2.74-8.83, P < 0.001), and prior antibiotics exposure in the preceding 12 months(OR 4.51, 95%CI 2.15-9.44, P < 0.001). For ILTCs, prior admission to AHs(OR 6.73, 95%CI 1.58-28.71, P = 0.010) and prior antibiotics exposure(OR 5.53, 95%CI 1.66-18.40, P = 0.005), presence of indwelling urinary catheter(OR 1.97, 95%CI 1.14-3.40, P = 0.014), and LOS >14 days(OR 0.47, 95%CI 0.26-0.83, P = 0.010) were associated with VRE colonization. Conclusion: Antibiotics exposure and hospitalization in an AH in the preceding 12 months were common risk factors for VRE colonization in the AH and ILTCs. Prior VRE carriage and LOS >14 days increased the risk of colonization in the AH. Presence of indwelling urinary catheter increased but LOS >14 days decreased the risk in ILTCs. Pre-emptive contact precautions and targeted screening could be implemented for these high-risk patients at AHs and ILTCs.

The local hospital milieu and healthcare-associated vancomycin-resistant enterococcus acquisition

Vancomycin-resistant enterococcus (VRE) causes 4% of all healthcare-associated infections in the USA. The process by which the local hospital milieu contributes to VRE acquisition is not fully understood. To determine the importance of specific factors within the local hospital environment for healthcare-associated VRE acquisition. This retrospective cohort study included patients admitted to six intensive care units at an academic medical centre from January 2012 to December 2016 with negative rectal VRE cultures on admission. VRE acquisition was defined as a positive surveillance swab performed at any time after the initial negative swab during the index hospitalization. The exposures of interest were VRE colonization pressure, VRE importation pressure, and use of vancomycin. Multivariable Cox proportional hazards modelling was performed, with patients followed until VRE acquisition, death, or for up to 30 days. Of 8485 patients who were initially VRE negative, 161 patients acquired VRE. On univariate analysis, patients with VRE acquisition were more likely to have received vancomycin, to have had a neighbouring patient who received vancomycin, to have high VRE importation pressure, or to have high VRE colonization pressure. On multivariable analysis, only high VRE colonization pressure was an independent predictor of VRE acquisition (adjusted hazard ratio: 1.79; 95% confidence interval: 1.19-2.70). VRE colonization pressure was the most important risk factor for healthcare-associated VRE acquisition, regardless of VRE importation pressure. Interventions seeking to reduce VRE acquisition should focus on minimizing transmission between patients with known VRE and the local hospital environment.

Gut colonization with vancomycin-resistant Enterococcus and risk for subsequent enteric infection

BackgroundGut colonization with vancomycin-resistant Enterococcus (VRE) is associated with poor outcomes. This study evaluated the impact of VRE colonization on subsequent acquisition of enteric pathogens.MethodsWe performed a retrospective cohort study of adults admitted to an ICU from 2012 to 2017 who were screened for VRE colonization and subsequently underwent stool testing with a gastrointestinal pathogen PCR panel (GI PCR) with or without PCR testing for Clostridium difficile. Our primary outcome was the presence of any enteric pathogen. Cox proportional hazards modeling was used to adjust for factors associated with enteric infection.ResultsOf 761 patients who underwent VRE screening and subsequent GI PCR, 131 (17%) were colonized with VRE. Patients with VRE colonization were less likely to test positive on GI PCR compared to patients without VRE (9.2% vs 18%, p = 0.01); specifically for E. coli species (p = 0.03) and viral (p = 0.04) enteric infections. In 716 patients who underwent C. difficile testing, there was a trend towards more C. difficile infections in patients colonized with VRE (15% vs 10%, p = 0.11). On multivariable analysis, patients with VRE had a decreased risk of a positive GI PCR (aHR 0.47, 95% CI 0.25–0.88, p = 0.02) but not C. difficile infection, effects which persisted during 5 years of follow-up. Among positive tests, there was a greater proportion of C. difficile with VRE (57% vs 28%, p < 0.01).ConclusionsVRE colonization was associated with a decreased risk of subsequent non-C. difficile enteric infection. VRE domination of the gut microbiome may protect against acquisition of common enteric pathogens.