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An estimated 20-30% of patients with primary Clostridium difficile infection (CDI) develop recurrent CDI (rCDI) within 2 weeks of completion of therapy. While the actual mechanism of recurrence remains unknown, a variety of risk factors have been suggested and studied. The aim of this systematic review and meta-analysis was to evaluate current evidence on the risk factors for rCDI. We searched MEDLINE and 5 other databases for subject headings and text related to rCDI. All studies investigating risk factors of rCDI in a multivariate model were eligible. Information on study design, patient population, and assessed risk factors were collected. Data were combined using a random-effects model and pooled relative risk ratios (RRs) were calculated. A total of 33 studies (n=18,530) met the inclusion criteria. The most frequent independent risk factors associated with rCDI were age≥65 years (risk ratio [RR], 1.63; 95% confidence interval [CI], 1.24-2.14; P=.0005), additional antibiotics during follow-up (RR, 1.76; 95% CI, 1.52-2.05; P<.00001), use of proton-pump inhibitors (PPIs) (RR, 1.58; 95% CI, 1.13-2.21; P=.008), and renal insufficiency (RR, 1.59; 95% CI, 1.14-2.23; P=.007). The risk was also greater in patients previously on fluoroquinolones (RR, 1.42; 95% CI, 1.28-1.57; P<.00001). Multiple risk factors are associated with the development of rCDI. Identification of modifiable risk factors and judicious use of antibiotics and PPI can play an important role in the prevention of rCDI.

Background Environmental 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. Methods The 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. Results On inoculated surfaces, application of Tru-D at a reflected dose of 22,000 μWs/cm 2 for ~45 minutes consistently reduced recovery of C. difficile spores and MRSA by >2-3 log 10 colony forming units (CFU)/cm 2 and of VRE by >3-4 log 10 CFU/cm 2 . Similar killing of MRSA and VRE was achieved in ~20 minutes at a reflected dose of 12,000 μWs/cm 2 , 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. Conclusions The 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.

The intestinal tract provides an important reservoir for many nosocomial pathogens, including Enterococcus species, Enterobacteriaciae, Clostridium difficile, and Candida species. These organisms share several common risk factors and often coexist in the intestinal tract. Disruption of normal barriers, such as gastric acidity and the indigenous microflora of the colon, facilitates overgrowth of pathogens. Factors such as fecal incontinence and diarrhea contribute to the subsequent dissemination of pathogens into the health care environment. Selective pressure exerted by antibiotics plays a particularly important role in pathogen colonization, and adverse effects associated with these agents often persist beyond the period of treatment. Infection-control measures that are implemented to control individual pathogens may have a positive or negative impact on efforts to control other pathogens that colonize the intestinal tract.

The 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. To 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. Colonization 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. Recovery 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.

Objective:We investigated the quality of life (QoL) of patients hospitalized with C. difficile infection (CDI).Design:Prospective survey study.Setting:US tertiary-care referral center, acute-care setting.Participants:Adults hospitalized with a diagnosis of CDI, defined as ≥3 episodes of unformed stool in 24 hours and a positive laboratory test for C. difficile.Methods:We surveyed patients from July 2019 to March 2020 using the disease-specific Cdiff32 questionnaire and the generic PROMIS GH survey. We compared differences in Cdiff32 scores among demographic and clinical subgroups (including CDI severity, CDI recurrence, and various comorbidities) using 2-sample t tests. We compared PROMIS GH scores to the general population T score of 50 using 1-sample t tests. We performed multivariable linear regression to identify predictors of Cdiff32 scores.Results:In total, 100 inpatients (mean age, 58.6 ±17.1 years; 53.0% male; 87.0% white) diagnosed with CDI completed QoL surveys. PROMIS GH physical health summary scores (T = 37.3; P < .001) and mental health summary scores (T = 43.4; P < .001) were significantly lower than those of the general population. In bivariate analysis, recurrent CDI, severe CDI, and number of stools were associated with lower Cdiff32 scores. In multivariable linear regression, recurrent CDI, severe CDI, and each additional stool in the previous 24 hours were associated with significantly decreased Cdiff32 scores.Conclusions:Patients hospitalized with CDI reported low scores on the Cdiff32 and PROMIS GH, demonstrating a negative impact of CDI on QoL in multiple health domains. The Cdiff32 questionnaire is particularly sensitive to QoL changes in patients with recurrent or severe disease.

Background. Asymptomatic fecal carriage of Clostridium difficile is common in patients staying in health care facilities, but the importance of asymptomatic carriers with regard to disease transmission is unclear. Methods. We prospectively examined the prevalence of asymptomatic carriage of epidemic North American pulsed-field gel electrophoresis type 1 and nonepidemic toxigenic C. difficile strains among long-term care patients in the context of an outbreak of C. difficile–associated disease and evaluated the frequency of skin and environmental contamination. Molecular typing was performed by pulsed-field gel electrophoresis. Logistic regression was used to assess factors associated with asymptomatic carriage, and a sensitive and specific prediction rule was developed to identify high-risk patients. Results. Thirty-five (51%) of 68 asymptomatic patients were carriers of toxigenic C. difficile, and 13 (37%) of these patients carried epidemic strains. Compared with noncarriers, asymptomatic carriers had higher percentages of skin (61% vs. 19%; P = .001) and environmental contamination (59% vs. 24%; P = .004). Eighty-seven percent of isolates found in skin samples and 58% of isolates found in environmental samples were identical to concurrent isolates found in stool samples. Spores on the skin of asymptomatic patients were easily transferred to investigators' hands. Previous C. difficile–associated disease (P < .001) and previous antibiotic use (P = .017) were associated with asymptomatic carriage, and the combination of these 2 variables was predictive of asymptomatic carriage (sensitivity, 77%; specificity, 58%; positive predictive value, 66%; negative predictive value, 70%). Conclusions. Our findings suggest that asymptomatic carriers of epidemic and nonepidemic C. difficile strains have the potential to contribute significantly to disease transmission in long-term care facilities. Clinical factors, such as previous C. difficile–associated disease and recent antibiotic use, may be predictive of asymptomatic carriage.

Personal protective equipment (PPE) is crucially important to the safety of both patients and medical personnel, particularly in the event of an infectious pandemic. As the incidence of Coronavirus Disease 2019 (COVID-19) increases exponentially in the United States and many parts of the world, healthcare provider demand for these necessities is currently outpacing supply. In the midst of the current pandemic, there has been a concerted effort to identify viable ways to conserve PPE, including decontamination after use. In this study, we outline a procedure by which PPE may be decontaminated using ultraviolet (UV) radiation in biosafety cabinets (BSCs), a common element of many academic, public health, and hospital laboratories. According to the literature, effective decontamination of N95 respirator masks or surgical masks requires UV-C doses of greater than 1 Jcm −2 , which was achieved after 4.3 hours per side when placing the N95 at the bottom of the BSCs tested in this study. We then demonstrated complete inactivation of the human coronavirus NL63 on N95 mask material after 15 minutes of UV-C exposure at 61 cm (232 μW cm −2 ). Our results provide support to healthcare organizations looking for methods to extend their reserves of PPE.

Antimicrobial therapy plays a central role in the pathogenesis of Clostridium difficile infection (CDI), presumably through disruption of indigenous intestinal microflora, thereby allowing C. difficile to grow and produce toxin. Investigations involving animal models and studies performed in vitro suggest that inhibitory activity against C. difficile and differences in the propensity to stimulate toxin production may also influence the likelihood that particular drugs may cause CDI. Although nearly all antimicrobial classes have been associated with CDI, clindamycin, third-generation cephalosporins, and penicillins have traditionally been considered to harbor the greatest risk. Recent studies have also implicated fluoroquinolones as high-risk agents, a finding that is most likely to be related in part to increasing fluoroquinolone resistance among epidemic strains (i.e., restriction-endonuclease analysis group BI/North American PFGE type 1 strains) and some nonepidemic strains of C. difficile. Restrictions in the use of clindamycin and third-generation cephalosporins have been associated with reductions in CDI. Because use of any antimicrobial has the potential to induce the onset of CDI and disease caused by other health care–associated pathogens, antimicrobial stewardship programs that promote judicious use of antimicrobials are encouraged in concert with environmental and infection control–related efforts.

To identify risk factors for asymptomatic Clostridioides difficile colonization among hospitalized adults utilizing a meta-analysis, which may enable early identification of colonized patients at risk of spreading C. difficile. Meta-analysis and systematic review. We systematically searched MEDLINE, Scopus, Web of Science, and EMBASE from January 1, 1975, to February 15, 2020, for articles related to C. difficile colonization among hospitalized adults. Studies with multivariable analyses evaluating risk factors for asymptomatic colonization were eligible. Among 5,506 studies identified in the search, 19 studies met the inclusion criteria. Included studies reported 20,334 adult patients of whom 1,588 were asymptomatically colonized with C. difficile. Factors associated with an increased risk of colonization were hospitalization in the previous 6 months (OR, 2.18; 95% CI, 1.86-2.56; P < .001), use of gastric acid suppression therapy within the previous 8 weeks (OR, 1.42; 95% CI, 1.17-1.73; P < .001), tube feeding (OR, 2.02; 95% CI, 1.06-3.85; P = .03), and corticosteroid use in the previous 8 weeks (OR, 1.58; 95% CI, 1.14-2.17; P = .006). Receipt of antibiotics in the previous 3 months (OR, 1.37; 95% CI, 0.94-2.01; P = .10) was not associated with statistically significant effects on risk of colonization. C. difficile colonization was significantly associated with previous hospitalization, gastric acid suppression, tube feeding, and corticosteroid use. Recognition of these risk factors may assist in identifying asymptomatic carriers of C. difficile and taking appropriate measures to reduce transmission.

To the Editor—Heating, ventilation, and air conditioning (HVAC) systems in healthcare facilities maintain the indoor air temperature and humidity at comfortable levels and provide adequate ventilation to control odors and reduce risk for transmission of airborne pathogens.1,2 Failure of the HVAC system or a temporary shutdown for maintenance could subject patients and staff to increased risk for exposure to airborne contaminants. [...]limited information is available on the infection control implications of temporary HVAC shutdowns.3 Therefore, we assessed ventilation during maintenance of the HVAC system in our hospital requiring 2 temporary shutdowns of the air handling system supplying one-half of the building. [...]temporary shutdown of an air handler for one-half of our hospital had only a modest impact on ventilation based on carbon dioxide monitoring and assessment of aerosol particle clearance.