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To determine whether hydrogen peroxide vapor (HPV) decontamination can reduce environmental contamination with and nosocomial transmission of Clostridium difficile.
A prospective before-after intervention study.
A hospital affected by an epidemic strain of C. difficile.
Intensive HPV decontamination of 5 high-incidence wards followed by hospital-wide decontamination of rooms vacated by patients with C. difficile-associated disease (CDAD). The preintervention period was June 2004 through March 2005, and the intervention period was June 2005 through March 2006.
Eleven (25.6%) of 43 cultures of samples collected by sponge from surfaces before HPV decontamination yielded C. difficile, compared with 0 of 37 cultures of samples obtained after HPV decontamination (P < .001). On 5 high-incidence wards, the incidence of nosocomial CDAD was significantly lower during the intervention period than during the preintervention period (1.28 vs 2.28 cases per 1,000 patient-days; P = .047). The hospital-wide CDAD incidence was lower during the intervention period than during the preintervention period (0.84 vs 1.36 cases per 1,000 patient-days; P = .26). In an analysis limited to months in which the epidemic strain was present during both the preintervention and the intervention periods, CDAD incidence was significandy lower during the intervention period than during the preintervention period (0.88 vs 1.89 cases per 1,000 patient-days; P = .047).
HPV decontamination was efficacious in eradicating C. difficile from contaminated surfaces. Further studies of the impact of HPV decontamination on nosocomial transmission of C. difficile are warranted.
Introduction
Changes in body temperature and metabolism (energy and substrate metabolism) are common features of many disease states, and have been well documented following various forms of tissue injury. Body temperature is a precisely regulated phenomenon such that core temperature (most probably brain temperature) is normally maintained within a narrow range by physiological controls operating on heat loss and heat production (metabolic rate). In contrast, energy metabolism is highly variable, depending on the balance between energy intake and expenditure (heat production and physical work). Nevertheless, there is extensive evidence that this balance between energy input and output remains remarkably constant over long periods of time in many organisms, including humans. Thus total body energy content, mainly in the form of fat and protein, can be stable for months or even years. The physiological regulation of body temperature and energy metabolism, which are both under direct control of the central nervous system (CNS), are closely related. The regulation of core temperature is achieved by controls operating on heat loss and heat production, with the latter predominating in many situations. Thus, development of fever is almost always associated with increased rates of heat production and, if sustained, these will lead to depletion of body energy stores and weight loss which are confounded by reduced levels of food intake. In contrast, increased heat production, if not fully compensated by enhanced heat loss, will lead to a rise in body temperature, although this does not necessarily manifest itself as ‘fever’ according to strict physiological definition.
For these reasons, the central control of body temperature and the metabolic rate response to injury will be considered in parallel. Alterations in specific nutrient metabolism (e.g. protein and lipid metabolism) following injury are numerous and complex, and will therefore not be reviewed in detail, although it is obvious that these both influence and are directly dependent on variations in core temperature and metabolic rate.
Basic aspects of thermoregulation and metabolic rate - definitions and measurement
Body temperature is most reliably determined from measurements of deep core temperature, i.e. gut or brain temperature. Rectal temperature can provide a reliable index of this parameter but is sometimes inconvenient, while oral temperature may be unreliable. In experimental animals, core temperature is usually determined by insertion of a thermocouple beyond the rectal sphincter into the colon.
To develop optical power limiting thin films prepared from water-soluble materials, we have prepared chromophore-doped gelatin thin films. Thin films of gelatin were prepared by spin coating followed by annealing. We also prepared thin films doped with the water-soluble chromophore copper phthalocyanine sodium tetrasulfonate. The films were characterized by film profilometry and optical absorption spectroscopy. Optical power limiting measurements of these films, as well as comparisons with aqueous solution and gels were performed.
To develop novel optical thin films, we have prepared self-assembled polypeptide films by an electrostatic process. The films were placed on a glass slide previously silanized by an amino silane and given a positive charge by immersion in aqueous acid. Subsequent immersion of the slide in aqueous anionic solutions of either poly(L-glutamic acid), congo red, copper phthalocyanine tetrasulfonic acid or p-nitroaniline-modified poly(L-glutamic acid) resulted in deposition of the anions on the surface. Following anionic immersion, the slides were dipped into a cationic poly(L-lysine) solution. Alternate dipping into anionic and cationic solutions yielded multilayers. The thin films were characterized by optical absorption and circular dichroism. The optical density increased with dipping cycles. Circular dichroism measurements of the thin films showed induced dichroism of the congo red and phthalocyanine-containing films, suggesting formation of a locally ordered dye-polypeptide complex. Solution circular dichroism measurements of the polypeptides indicated a coil conformation, while poly(Lglutamic acid)/poly(L-lysine) complexes showed circular dichroism spectrum characteristic of a β-sheet.
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