A randomized controlled trial of Lactobacillus rhamnosus GG on antimicrobial-resistant organism colonization.

OBJECTIVE: Alteration of the colonic microbiota following antimicrobial exposure allows colonization by antimicrobial-resistant organisms (AROs). Ingestion of a probiotic, such as Lactobacillus rhamnosus GG (LGG), could prevent colonization or infection with AROs by promoting healthy colonic microbiota. The purpose of this trial was to determine the effect of LGG administration on ARO colonization in hospitalized patients receiving antibiotics. DESIGN: Prospective, double-blinded, randomized controlled trial of LGG versus placebo among patients receiving broad-spectrum antibiotics. SETTING: Tertiary care center. PATIENTS: In total, 88 inpatients receiving broad-spectrum antibiotics were enrolled. INTERVENTION: Patients were randomized to receive 1 capsule containing 1×1010 cells of LGG twice daily (n = 44) or placebo (n = 44), stratified by ward type. Stool or rectal-swab specimens were collected for culture at enrollment, during admission, and at discharge. Using selective media, specimens were cultured for Clostridioides difficile, vancomycin-resistant Enterococcus spp (VRE), and antibiotic-resistant gram-negative bacteria. The primary outcome was any ARO acquisition. Secondary outcomes included loss of any ARO if colonized at enrollment, and acquisition or loss of individual ARO. RESULTS: ARO colonization prevalence at study enrollment was similar (LGG 39% vs placebo 39%). We detected no difference in any ARO acquisition (LGG 30% vs placebo 33%; OR,1.19; 95% CI, 0.38-3.75) nor for any individual ARO acquisition. There was no difference in the loss of any ARO (LGG 18% vs placebo 24%; OR, 1.44; 95% CI, 0.27-7.68) nor for any individual ARO. CONCLUSION: LGG administration neither prevented acquisition of ARO nor accelerated loss of ARO colonization.

An Evaluation of Food as a Potential Source for Clostridium difficile Acquisition in Hospitalized Patients.

OBJECTIVE To determine whether Clostridium difficile is present in the food of hospitalized patients and to estimate the risk of subsequent colonization associated with C. difficile in food. METHODS This was a prospective cohort study of inpatients at a university-affiliated tertiary care center, May 9, 2011-July 12, 2012. Enrolled patients submitted a portion of food from each meal. Patient stool specimens and/or rectal swabs were collected at enrollment, every 3 days thereafter, and at discharge, and were cultured for C. difficile. Clinical data were reviewed for evidence of infection due to C. difficile. A stochastic, discrete event model was developed to predict exposure to C. difficile from food, and the estimated number of new colonization events from food exposures per 1,000 admissions was determined. RESULTS A total of 149 patients were enrolled and 910 food specimens were obtained. Two food specimens from 2 patients were positive for C. difficile (0.2% of food samples; 1.3% of patients). Neither of the 2 patients was colonized at baseline with C. difficile. Discharge colonization status was available for 1 of the 2 patients and was negative. Neither was diagnosed with C. difficile infection while hospitalized or during the year before or after study enrollment. Stochastic modeling indicated contaminated hospital food would be responsible for less than 1 newly colonized patient per 1,000 hospital admissions. CONCLUSIONS The recovery of C. difficile from the food of hospitalized patients was rare. Modeling suggests hospital food is unlikely to be a source of C. difficile acquisition. Infect Control Hosp Epidemiol 2016;1401-1407.

Randomized Controlled Trial to Determine the Impact of Probiotic Administration on Colonization With Multidrug-Resistant Organisms in Critically Ill Patients.

This was a randomized controlled pilot study of Lactobacillus rhamnosus GG versus standard of care to prevent gastrointestinal multidrug-resistant organism colonization in intensive care unit patients. Among 70 subjects, there were no significant differences in acquisition or loss of any multidrug-resistant organisms (P>.05) and no probiotic-associated adverse events.

Prevalence and risk factors for asymptomatic Clostridium difficile carriage.

BACKGROUND: Clostridium difficile infection (CDI) incidence has increased dramatically over the last decade. Recent studies suggest that asymptomatic carriers may be an important reservoir of C. difficile in healthcare settings. We sought to identify the prevalence and risk factors for asymptomatic C. difficile carriage on admission to the hospital. METHODS: Patients admitted to Barnes-Jewish Hospital without diarrhea were enrolled from June 2010 through October 2011. Demographic information and healthcare and medication exposures 90 days prior to admission were collected. Stool specimens or rectal swabs were collected within 48 hours of admission and stored at -30°C until cultured. Clostridium difficile isolates were typed and compared with isolates from patients with CDI. RESULTS: A stool/swab specimen was obtained for 259 enrolled subjects on admission. Two hundred four (79%) were not colonized, 40 (15%) had toxigenic C. difficile (TCD), and 15 (6%) had nontoxigenic C. difficile. There were no differences between TCD-colonized and -uncolonized subjects for age (mean, 56 vs 58 years; P = .46), comorbidities, admission from another healthcare facility (33% vs 24%; P = .23), or recent hospitalization (50% vs 50%; P = .43). There were no differences in antimicrobial exposures in the 90 days prior to admission (55% vs 56%; P = .91). Asymptomatic carriers were colonized with strains similar to strains from patients with CDI, but the relative proportions were different. CONCLUSIONS: There was a high prevalence of TCD colonization on admission. In contrast to past studies, TCD colonization was not associated with recent antimicrobial or healthcare exposures. Additional investigation is needed to determine the role of asymptomatic TCD carriers on hospital-onset CDI incidence.

The influence of infection on hospital mortality for patients requiring > 48 h of intensive care.

OBJECTIVE: To determine the influence of microbiologically confirmed infection on hospital mortality among patients requiring intensive care for > 48 h. DESIGN: Prospective cohort study. SETTING: Medical ICU of the Barnes-Jewish Hospital, an urban teaching hospital. PATIENTS: A total of 893 patients requiring intensive care for > 48 h. INTERVENTIONS: Prospective patient surveillance and data collection. MEASUREMENTS AND MAIN RESULTS: Three hundred seventy-two patients (41.7%) requiring intensive care for > 48 h had a microbiologically confirmed infection. Only six patients (0.7% [1.6% of patients with microbiologically confirmed infections]) received inadequate antimicrobial therapy during the first 24 h of treatment, and 248 patients (27.8%) died during hospitalization. Compared to hospital survivors, hospital nonsurvivors were significantly more likely to have a microbiologically confirmed infection (53.2% vs 37.2%, respectively; p < 0.001) and to develop severe sepsis (45.6% vs 28.7%, respectively; p < 0.001). Cirrhosis and the requirement for vasopressors were the only variables identified by multiple logistic regression analysis as independent risk factors for hospital mortality in all patient groupings of severity of illness. Multiple logistic regression analysis also demonstrated that underlying malignancy (adjusted odds ratio [AOR], 1.98; 95% CI, 1.55 to 2.53), chronic renal insufficiency (AOR, 1.57; 95% CI, 1.31 to 1.87), cirrhosis (AOR, 1.94; 95% CI, 1.48 to 2.53), temperature > 38.3 degrees C (AOR, 1.72; 95% CI, 1.47 to 2.02), severe sepsis (AOR, 2.78; 95% CI, 1.94 to 3.98), positive culture for vancomycin-resistant enterococci (AOR, 1.78; 95% CI, 1.51 to 2.09), and the presence of multiple infections (AOR, 1.65; 95% CI, 1.28 to 2.14) were independently associated with the requirement for therapy with vasopressors. CONCLUSIONS: Microbiologically confirmed infections are common among patients requiring medical intensive care for > 48 h. Despite the administration of adequate antimicrobial therapy, microbiologically confirmed infections appear to be an important cause of hemodynamic instability and increased hospital mortality. These data suggest that clinical efforts aimed at the prevention of infections and improvements in the medical management of patients with severe infections, especially those associated with hemodynamic instability and the need for vasopressors, are required to achieve further improvements in patient outcomes.

The epidemiology of vancomycin-resistant Enterococcus colonization in a medical intensive care unit.

OBJECTIVE: To determine the epidemiology of colonization with vancomycin-resistant Enterococcus (VRE) among intensive care unit (ICU) patients. DESIGN: Ten-month prospective cohort study. SETTING: A 19-bed medical ICU of a 1,440-bed teaching hospital. METHODS: Patients admitted to the ICU had rectal swab cultures for VRE on admission and weekly thereafter. VRE-positive patients were cared for using contact precautions. Clinical data, including microbiology reports, were collected prospectively during the ICU stay. RESULTS: Of 519 patients who had admission stool cultures, 127 (25%) had cultures that were positive for VRE. Risk factors for VRE colonization identified by multiple logistic regression analysis were hospital stay greater than 3 days prior to ICU admission (adjusted odds ratio [AOR], 3.6; 95% confidence interval [CI95], 2.3 to 5.7), chronic dialysis (AOR, 2.4; CI95, 1.2 to 4.5), and having been admitted to the study hospital one to two times (AOR, 2.3; CI95, 1.4 to 3.8) or more than two times (AOR, 6.5; CI95, 3.7 to 11.6) within the past 12 months. Of the 352 VRE-negative patients who had one or more follow-up cultures, 74 (21%) became VRE positive during their ICU stay (27 cases per 1,000 patient-ICU days). CONCLUSION: The prevalence of VRE culture positivity on ICU admission was high and a sizable fraction of ICU patients became VRE positive during their ICU stay despite contact precautions for VRE-positive patients. This was likely due in large part to prior VRE exposures in the rest of the hospital where these control measures were not being used.