Self-Disinfecting Copper Beds Sustain Terminal Cleaning and Disinfection Effects throughout Patient Care.

Microbial burden associated with near-patient touch surfaces results in a greater risk of health care-associated infections (HAIs). Acute care beds may be a critical fomite, as traditional plastic surfaces harbor the highest concentrations of bacteria associated with high-touch surfaces in a hospital room's patient zone. Five high-touch intensive care unit (ICU) bed surfaces encountered by patients, health care workers, and visitors were monitored by routine culture to assess the effect U.S. Environmental Protection Agency (U.S. EPA)-registered antimicrobial copper materials have on the microbial burden. Despite both daily and discharge cleaning and disinfection, each control bed's plastic surfaces exceeded bacterial concentrations recommended subsequent to terminal cleaning and disinfection (TC&D) of 2.5 aerobic CFU/cm2 Beds with self-disinfecting (copper) surfaces harbored significantly fewer bacteria throughout the patient stay than control beds, at levels below those considered to increase the likelihood of HAIs. With adherence to routine daily and terminal cleaning regimes throughout the study, the copper alloy surfaces neither tarnished nor required additional cleaning or special maintenance. Beds encapsulated with U.S. EPA-registered antimicrobial copper materials were found to sustain the microbial burden below the TC&D risk threshold levels throughout the patient stay, suggesting that outfitting acute care beds with such materials may be an important supplement to controlling the concentration of infectious agents and thereby potentially reducing the overall HAI risk.IMPORTANCE Despite cleaning efforts of environmental service teams and substantial compliance with hand hygiene best practices, the microbial burden in patient care settings often exceeds concentrations at which transfer to patients represents a substantial acquisition risk for health care-associated infections (HAIs). Approaches to limit HAI risk have relied on designing health care equipment and furnishings that are easier to clean and/or the use of no-touch disinfection interventions such as germicidal UV irradiation or vapor deposition of hydrogen peroxide. In a clinical trial evaluating the largest fomite in the patient care setting, the bed, a bed was encapsulated with continuously disinfecting antimicrobial copper surfaces, which reduced the bacteria on surfaces by 94% and sustained the microbial burden below the terminal cleaning and disinfection risk threshold throughout the patient's stay. Such an intervention, which continuously limits microbes on high-touch surfaces, should be studied in a broader range of health care settings to determine its potential long-range efficacy for reducing HAI.

In situ evaluation of a persistent disinfectant provides continuous decontamination within the clinical environment.

Microbial bioburden associated with the built environment can impact the rate of health care-associated infection acquisition; higher bioburden results in a greater incidence of health care-associated infections. Two disinfectants registered by the US Environmental Protection Agency and a trial disinfectant were evaluated for their ability to limit the establishment of bioburden subsequent to application under in situ conditions on patient bed rails within a medical intensive care unit. Bioburden samples were collected immediately prior to disinfection and at 1, 6, and 24 hours after application. The trial disinfectant was engineered to provide continuous disinfection over a 24-hour period. Each disinfectant was able to significantly control bioburden for the first hour. In comparison, the persistent agent was found superior for all time points when compared to a dilutable quaternary ammonium agent, and it was significantly better for controlling bioburden for 2 of the 3 times points for the disinfectant with ethanol and quaternary ammonium as its agent.

Antimicrobial copper alloys decreased bacteria on stethoscope surfaces.

BACKGROUND: Stethoscopes may serve as vehicles for transmission of bacteria among patients. The aim of this study was to assess the efficacy of antimicrobial copper surfaces to reduce the bacterial concentration associated with stethoscope surfaces. METHODS: A structured prospective trial involving 21 health care providers was conducted at a pediatric emergency division (ED) (n = 14) and an adult medical intensive care unit located in tertiary care facilities (n = 7). Four surfaces common to a stethoscope and a facsimile instrument fabricated from U.S. Environmental Protection Agency-registered antimicrobial copper alloys (AMCus) were assessed for total aerobic colony counts (ACCs), methicillin-resistant Staphylococcus aureus, gram-negative bacteria, and vancomycin-resistant enterococci for 90 days. RESULTS: The mean ACCs collectively recovered from all stethoscope surfaces fabricated from the AMCus were found to carry significantly lower concentrations of bacteria (pediatric ED, 11.7 vs 127.1 colony forming units [CFU]/cm2, P < .00001) than their control equivalents. This observation was independent of health care provider or infection control practices. Absence of recovery of bacteria from the AMCu surfaces (66.3%) was significantly higher (P < .00001) than the control surfaces (22.4%). The urethane rim common to the stethoscopes was the most heavily burdened surface; mean concentrations exceeded the health care-associated infection acquisition concentration (5 CFU/cm2) by at least 25×, supporting that the stethoscope warrants consideration in plans mitigating microbial cross-transmission during patient care. CONCLUSIONS: Stethoscope surfaces fabricated with AMCus were consistently found to harbor fewer bacteria.

Copper continuously limits the concentration of bacteria resident on bed rails within the intensive care unit.

Cleaning is an effective way to lower the bacterial burden (BB) on surfaces and minimize the infection risk to patients. However, BB can quickly return. Copper, when used to surface hospital bed rails, was found to consistently limit surface BB before and after cleaning through its continuous antimicrobial activity.

Sustained reduction of microbial burden on common hospital surfaces through introduction of copper.

The contribution of environmental surface contamination with pathogenic organisms to the development of health care-associated infections (HAI) has not been well defined. The microbial burden (MB) associated with commonly touched surfaces in intensive care units (ICUs) was determined by sampling six objects in 16 rooms in ICUs in three hospitals over 43 months. At month 23, copper-alloy surfaces, with inherent antimicrobial properties, were installed onto six monitored objects in 8 of 16 rooms, and the effect that this application had on the intrinsic MB present on the six objects was assessed. Census continued in rooms with and without copper for an additional 21 months. In concert with routine infection control practices, the average MB found for the six objects assessed in the clinical environment during the preintervention phase was 28 times higher (6,985 CFU/100 cm(2); n = 3,977 objects sampled) than levels proposed as benign immediately after terminal cleaning (<250 CFU/100 cm(2)). During the intervention phase, the MB was found to be significantly lower for both the control and copper-surfaced objects. Copper was found to cause a significant (83%) reduction in the average MB found on the objects (465 CFU/100 cm(2); n = 2714 objects) compared to the controls (2,674 CFU/100 cm(2); n = 2,831 objects [P < 0.0001]). The introduction of copper surfaces to objects formerly covered with plastic, wood, stainless steel, and other materials found in the patient care environment significantly reduced the overall MB on a continuous basis, thereby providing a potentially safer environment for hospital patients, health care workers (HCWs), and visitors.

Intrinsic bacterial burden associated with intensive care unit hospital beds: effects of disinfection on population recovery and mitigation of potential infection risk.

BACKGROUND: Commonly touched items are likely reservoirs from which patients, health care workers, and visitors may encounter and transfer microbes. A quantitative assessment was conducted of the risk represented by the intrinsic bacterial burden associated with bed rails in a medical intensive care unit (MICU), and how disinfection might mitigate this risk. METHODS: Bacteria present on the rails from 36 patient beds in the MICU were sampled immediately before cleaning and at 0.5, 2.5, 4.5, and 6.5 hours after cleaning. Beds were sanitized with either a bottled disinfectant (BD; CaviCide) or an automated bulk-diluted disinfectant (ABDD; Virex II 256). RESULTS: The majority of bacteria recovered from the bed rails in the MICU were staphylococci, but not methicillin-resistant Staphylococcus aureus. Vancomycin-resistant enterococci were recovered from 3 beds. Bottled disinfectant reduced the average bacterial burden on the rails by 99%. However, the burden rebounded to 30% of that found before disinfection by 6.5 hours after disinfection. ABDD reduced the burden by an average of 45%, but levels rebounded within 2.5 hours. The effectiveness of both disinfectants was reflected in median reductions to burden of 98% for BD and 95% for ABDD. CONCLUSIONS: Cleaning with hospital-approved disinfectants reduced the intrinsic bacterial burden on bed rail surfaces by up to 99%, although the population, principally staphylococci, rebounded quickly to predisinfection levels.

Patient environment microbial burden reduction: a pilot study comparison of 2 terminal cleaning methods.

Effective cleaning of the patient environment has been advocated to reduce the risk for nosocomial infection. This pilot study compared 2 terminal cleaning methods, a traditional method in which a disinfectant was applied with a wetted cloth and an alternative method in which the disinfectant was applied using the PureMist system (PureCart Systems, Green Bay, WI). There was no difference in effectiveness, with a mean relative reduction of microbial burden of 84% for the traditional method versus 88% for the PureMist method.

Versican proteolysis mediates myocardial regression during outflow tract development.

An important phase of cardiac outflow tract (OFT) formation is the remodeling of the distal region of the common outlet in which the myocardial sleeve is replaced by with smooth muscle. Here we demonstrate that expression of the proteoglycan versican is reduced before the loss of myocardium from the distal cardiac outlet concomitant with an increase in production of the N-terminal cleavage fragment of versican. To test whether versican proteolysis plays a role in OFT remodeling, we determined the effects of adenoviral-mediated expression of a versican isoform devoid of known matrix metalloproteinase cleavage sites (V3) and an N-terminal fragment of versican (G1). V3 expression promoted an increase in thickness of the proximal OFT myocardial layer independent of proliferation. In contrast, the G1 domain caused thinning and interruptions of the OFT myocardium. These in vivo findings were consistent with findings using cultured primary cardiomyocytes showing that the V3 promoted myocardial cell-cell association while the G1 domain caused a loss of myocardial cell-cell association. Taken together, we conclude that intact versican and G1-containing versican cleavage products have opposing effects on myocardial cells and that versican proteolysis may facilitate the loss of distal myocardium during OFT remodeling.

Proteolytic cleavage of versican during cardiac cushion morphogenesis.

The proteoglycan versican is essential to the formation of endocardial cushion mesenchyme by epithelial-mesenchymal transformation (EMT). A potentially important factor in the regulation of versican activity during cushion EMT is proteolysis by ADAMTS metalloproteinases. Using antibodies to the DPEAAE neoepitope created by ADAMTS proteolysis of versican, we detected the amino terminal 70-kDa versican cleavage fragment in cardiac cushions. Initially (i.e., 9.5 days post coitum [dpc]), the fragment is associated with endocardial cells undergoing EMT and with newly derived mesenchymal cells. ADAMTS-1 and its cofactor fibulin-1 were also associated with these cells. As cushions become increasingly populated with mesenchymal cells (10.5-12.5 dpc), the fragment remains asymmetrically distributed compared with the pattern of total versican. Highest levels of the fragment are present in regions immediately subjacent to the endocardium characterized as having densely packed, rounded cells, lacking cellular protrusions. With further development (i.e., 12.5-14.5 dpc), the pattern of fragment distribution within cushions broadens to include the ECM surrounding loosely packed mesenchymal cells in the cushion core. Together, the findings reveal that versican proteolysis leading to the production of the 70-kDa fragment is integral to the formation and differentiation of endocardial cushion mesenchyme.

Normal distribution of melanocytes in the mouse heart.

We report the consistent distribution of a population of pigmented trp-1-positive cells in several important septal and valvular structures of the normal mouse (C57BL/6) heart. The pigmented cell population was first apparent by E16.5 p.c. in the right atrial wall and extended into the atrium along the interatrial septum. By E17.5, these cells were found along the apical membranous interventricular septum near or below the surface of the endocardium. The most striking distribution of dark pigmented cells was found in the tricuspid and mitral valvular leaflets and chordae tendineae. The normal distribution of pigmented cells in the valvuloseptal apparatus of C57BL/6 adult heart suggests that a premelanocytic lineage may participate in the earlier morphogenesis of the valve leaflets and chordae tendineae. The origin of the premelanocyte lineage is currently unknown. The most likely candidate populations include the neural crest and the epicardially derived cells. The only cell type in the heart previously shown to form melanocytes is the neural crest. The presence of neural crest cells, but not melanocytes, in some of the regions we describe has been reported by others. However, previous reports have not shown a contribution of melanocytes or neural crest derivatives to the atrioventricular valve leaflets or chordae tendineae in mouse hearts. If these cells are of neural crest origin, it would suggest a possibly greater contribution and persistence of neural crest cells to the valvuloseptal apparatus than has been previously understood.