BackgroundEnvironmental surfaces play an important role in transmission of healthcare-associated pathogens. There is a need for new disinfection methods that are effective against Clostridium difficile spores, but also safe, rapid, and automated.MethodsThe Tru-D™ Rapid Room Disinfection device is a mobile, fully-automated room decontamination technology that utilizes ultraviolet-C irradiation to kill pathogens. We examined the efficacy of environmental disinfection using the Tru-D device in the laboratory and in rooms of hospitalized patients. Cultures for C. difficile, methicillin-resistant Staphylococcus aureus (MRSA), and vancomycin-resistant Enterococcus (VRE) were collected from commonly touched surfaces before and after use of Tru-D.ResultsOn inoculated surfaces, application of Tru-D at a reflected dose of 22,000 μWs/cm2 for ~45 minutes consistently reduced recovery of C. difficile spores and MRSA by >2-3 log10 colony forming units (CFU)/cm2 and of VRE by >3-4 log10 CFU/cm2. Similar killing of MRSA and VRE was achieved in ~20 minutes at a reflected dose of 12,000 μWs/cm2, but killing of C. difficile spores was reduced. Disinfection of hospital rooms with Tru-D reduced the frequency of positive MRSA and VRE cultures by 93% and of C. difficile cultures by 80%. After routine hospital cleaning of the rooms of MRSA carriers, 18% of sites under the edges of bedside tables (i.e., a frequently touched site not easily amenable to manual application of disinfectant) were contaminated with MRSA, versus 0% after Tru-D (P < 0.001). The system required <5 minutes to set up and did not require continuous monitoring.ConclusionsThe Tru-D Rapid Room Disinfection device is a novel, automated, and efficient environmental disinfection technology that significantly reduces C. difficile, VRE and MRSA contamination on commonly touched hospital surfaces.

Background:The incidence and severity of Clostridium difficile infection (CDI) is increasing among adults; however, little is known about the epidemiology of CDI among children. Methods: We conducted a nested case-control study to identify the risk factors for and a prospective cohort study to determine the outcomes associated with severe CDI at 2 children's hospitals. Severe CDI was defined as CDI and at least 1 complication or Ն2 laboratory or clinical indicators consistent with severe disease. Studied outcomes included relapse, treatment failure, and CDI-related complications. Isolates were tested to determine North American pulsed-field gel electrophoresis type 1 lineage. Results: We analyzed 82 patients with CDI, of whom 48 had severe disease. Median age in years was 5.93 (1.78 -12.16) and 1.83 (0.67-8.1) in subjects with severe and nonsevere CDI, respectively (P ϭ 0.012). All patients with malignancy and CDI had severe disease. Nine subjects (11%) had North American pulsed-field gel electrophoresis type 1 isolates. Risk factors for severe disease included age (adjusted odds ratio ͓95% confidence interval͔: 1.12 ͓1.02, 1.24͔) and receipt of 3 antibiotic classes in the 30 days before infection (3.95 ͓1.19, 13.11͔). If infants less than 1 year of age were excluded, only receipt of 3 antibiotic classes remained significantly associated with severe disease. Neither the rate of relapse nor treatment failure differed significantly between patients with severe and nonsevere CDI. There was 1 death. Conclusions: Increasing age and exposure to multiple antibiotic classes were risk factors for severe CDI. Although most patients studied had severe disease, complications were infrequent. Relapse rates were similar to those reported in adults.

objective. To determine the effectiveness of a pulsed xenon ultraviolet (PX-UV) disinfection device for reduction in recovery of healthcareassociated pathogens.setting. Two acute-care hospitals.methods. We examined the effectiveness of PX-UV for killing of Clostridium difficile spores, methicillin-resistant Staphylococcus aureus (MRSA), and vancomycin-resistant Enterococcus (VRE) on glass carriers and evaluated the impact of pathogen concentration, distance from the device, organic load, and shading from the direct field of radiation on killing efficacy. We compared the effectiveness of PX-UV and ultraviolet-C (UV-C) irradiation, each delivered for 10 minutes at 4 feet. In hospital rooms, the frequency of native pathogen contamination on high-touch surfaces was assessed before and after 10 minutes of PX-UV irradiation.results. On carriers, irradiation delivered for 10 minutes at 4 feet from the PX-UV device reduced recovery of C. difficile spores, MRSA, and VRE by 0.55 ± 0.34, 1.85 ± 0.49, and 0.6 ± 0.25 log 10 colony-forming units (CFU)/cm 2 , respectively. Increasing distance from the PX-UV device dramatically reduced killing efficacy, whereas pathogen concentration, organic load, and shading did not. Continuous UV-C achieved significantly greater log 10 CFU reductions than PX-UV irradiation on glass carriers. On frequently touched surfaces, PX-UV significantly reduced the frequency of positive C. difficile, VRE, and MRSA culture results.conclusions. The PX-UV device reduced recovery of MRSA, C. difficile, and VRE on glass carriers and on frequently touched surfaces in hospital rooms with a 10-minute UV exposure time. PX-UV was not more effective than continuous UV-C in reducing pathogen recovery on glass slides, suggesting that both forms of UV have some effectiveness at relatively short exposure times. 2015;36(2):192-197 Automated room disinfection technologies are increasingly being used as an adjunct to standard cleaning and disinfection in healthcare facilities. Ultraviolet (UV) radiation devices have been most widely adopted owing to the efficiency and welldocumented efficacy of UV irradiation. Infect Control Hosp Epidemiol1-7 Several UV room disinfection devices are now being marketed. Most of these devices use low pressure mercury gas bulbs, but recently pulsed xenon flash bulbs have also been incorporated into disinfection systems. UV radiation has peak germicidal effectiveness in the wavelength range from 240 to 280 nm.

In an observational study with a limited number of subjects, a majority of patients with C. difficile-associated disease responded to therapy with metronidazole or vancomycin. Failure with metronidazole treatment may be attributable to a slower and less consistent microbiological response than that with oral vancomycin treatment.

Fidaxomicin causes less disruption of anaerobic microbiota during treatment of Clostridium difficile infection (CDI) than vancomycin and has activity against many vancomycin-resistant enterococci (VRE). In conjunction with a multicenter randomized trial of fidaxomicin versus vancomycin for CDI treatment, we tested the hypothesis that fidaxomicin promotes VRE and Candida species colonization less than vancomycin. Stool was cultured for VRE and Candida species before and after therapy. For patients with negative pretreatment cultures, the incidence of VRE and Candida species acquisition was compared. For those with preexisting VRE, the change in concentration during treatment was compared. The susceptibility of VRE isolates to fidaxomicin was assessed. Of 301 patients, 247 (82%) had negative VRE cultures and 252 (84%) had negative Candida species cultures before treatment. In comparison with vancomycin-treated patients, fidaxomicin-treated patients had reduced acquisition of VRE (7% vs 31%, respectively; P < .001) and Candida species (19% vs 29%, respectively; P = .03). For patients with preexisting VRE, the mean concentration decreased significantly in the fidaxomicin group (5.9 vs 3.8 log10 VRE/g stool; P = .01) but not the vancomycin group (5.3 vs 4.2 log10 VRE/g stool; P = .20). Most VRE isolates recovered after fidaxomicin treatment had elevated fidaxomicin minimum inhibitory concentrations (MICs; MIC90, 256 µg/mL), and subpopulations of VRE with elevated fidaxomicin MICs were common before therapy. Fidaxomicin was less likely than vancomycin to promote acquisition of VRE and Candida species during CDI treatment. However, selection of preexisting subpopulations of VRE with elevated fidaxomicin MICs was common during fidaxomicin therapy.Clinical Trials Registration. NCT00314951.

BackgroundThe intestinal microbiota protect the host against enteric pathogens through a defense mechanism termed colonization resistance. Antibiotics excreted into the intestinal tract may disrupt colonization resistance and alter normal metabolic functions of the microbiota. We used a mouse model to test the hypothesis that alterations in levels of bacterial metabolites in fecal specimens could provide useful biomarkers indicating disrupted or intact colonization resistance after antibiotic treatment.MethodsTo assess in vivo colonization resistance, mice were challenged with oral vancomycin-resistant Enterococcus or Clostridium difficile spores at varying time points after treatment with the lincosamide antibiotic clindamycin. For concurrent groups of antibiotic-treated mice, stool samples were analyzed using quantitative real-time polymerase chain reaction to assess changes in the microbiota and using non-targeted metabolic profiling. To assess whether the findings were applicable to another antibiotic class that suppresses intestinal anaerobes, similar experiments were conducted with piperacillin/tazobactam.ResultsColonization resistance began to recover within 5 days and was intact by 12 days after clindamycin treatment, coinciding with the recovery bacteria from the families Lachnospiraceae and Ruminococcaceae, both part of the phylum Firmicutes. Clindamycin treatment caused marked changes in metabolites present in fecal specimens. Of 484 compounds analyzed, 146 (30%) exhibited a significant increase or decrease in concentration during clindamycin treatment followed by recovery to baseline that coincided with restoration of in vivo colonization resistance. Identified as potential biomarkers of colonization resistance, these compounds included intermediates in carbohydrate or protein metabolism that increased (pentitols, gamma-glutamyl amino acids and inositol metabolites) or decreased (pentoses, dipeptides) with clindamycin treatment. Piperacillin/tazobactam treatment caused similar alterations in the intestinal microbiota and fecal metabolites.ConclusionsRecovery of colonization resistance after antibiotic treatment coincided with restoration of several fecal bacterial metabolites. These metabolites could provide useful biomarkers indicating intact or disrupted colonization resistance during and after antibiotic treatment.

Both for epidemiologic studies and for diagnostic testing, there is a need for effective, economical, and readily available selective media for the culture of Clostridium difficile. We have developed a reduced-cost substitute for cycloserine-cefoxitin-fructose agar (CCFA), which is an effective but expensive selective medium for C. difficile. The modified medium, called C. difficile brucella agar (CDBA), includes an enriched brucella base as a substitute for proteose peptone no. 2, and the concentration of sodium taurocholate has been reduced from 0.1% to 0.05%. To compare the sensitivities and selectivities of CDBA and CCFA, cultures for C. difficile were performed using stool samples from patients with C. difficile-associated disease. CDBA was as sensitive as CCFA for the recovery of C. difficile, with a similar frequency of breakthrough growth of stool microflora (25% versus 31%, respectively). A liquid formulation of the modified medium, termed C. difficile brucella broth (CDBB), stimulated rapid germination and outgrowth of C. difficile spores, at a rate comparable to that in cycloserine-cefoxitin-fructose broth. Our results suggest that CDBA and CDBB are sensitive, selective, and reduced-cost media for the recovery of C. difficile from stool samples.

No abstract