Multidose vial transmits HCV.
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Biomedical subjects
Publications and source records attributed to M S Favero.
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OBJECTIVE: To determine the susceptibilities of vancomycin-resistant and -sensitive enterococci (VRE and VSE) to various concentrations of commonly used, commercial, hospital-grade disinfectants. DESIGN: A microbial suspension test using inocula of 10(8) cells per mL in a disinfectant test dilution was used to determine inactivation kinetics of the test strains. In each test, 1-mL aliquots were removed from the cell-disinfectant mixtures at 15 and 30 seconds and then at 1-minute intervals for 5 minutes and neutralized. Appropriate serial dilutions were plated on agar medium for enumeration of survivors. RESULTS: VRE and VSE challenge inocula (in the absence of any additional protein or serum challenge) were below the limit of detection (5 colony-forming units/mL) after 15 seconds' exposure to the manufacturers' suggested use-dilutions of quaternary ammonium, phenolic, or iodophor germicidal detergents. In subsequent tests, when the disinfectants were diluted far beyond-the recommended use-dilutions (extended dilution), no differences were demonstrated between the susceptibilities of VRE and VSE. CONCLUSIONS: VRE and VSE are sensitive to a spectrum of commonly used environmental disinfectants and have parallel inactivation rates when challenged with extended dilutions of these products. Our findings did not demonstrate a relationship between antibiotic and germicide resistance. Routine disinfection and housekeeping protocols presently used in hospitals need not be altered due to concerns about the potential for environmentally mediated transmission of antibiotic-resistant microorganisms.
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In this study, fixation of attached glycocalyx on the interior surfaces of polyvinyl chloride distribution pipe remnants was compared with and without ruthenium red/osmium tetroxide and, in the final preparatory phase, with chemical dehydration and critical point drying. SEM examination of interior surface of the polyvinyl chloride pipe showed varying concentrations of adherent bacteria, depending on the preparatory technique used. It was concluded that using a combination of ruthenium red/osmium tetroxide and critical point drying is the optimum method for visually demonstrating aging biofilm on the interior surface of contaminated polyvinyl chloride pipe.
Publicity about human immunodeficiency virus (HIV) infection in athletes has focused attention on the potential for transmission of blood-borne pathogens during sports and athletic competitions. Existing information suggests that the potential risk for such transmission is extremely low and that the principal risks athletes have for acquiring HIV and hepatitis B virus are related to off-the-field activities. Therefore, efforts to prevent transmission of blood-borne pathogens among athletes should emphasize prevention in off-the-field settings. We summarize technical and other information about this issue, and provide recommendations for the education of sports participants, for infection control in athletic settings, and for training of coaches and officials.
Bloodborne pathogens are transmitted from person to person by sexual contact and by injection of drugs and, in health-care settings, by needlesticks and, in the case of HBV, by mucous membrane exposure. Conventional disinfection and sterilization and housekeeping strategies are sufficient for the environmental control of bloodborne viruses. Environmentally mediated infection transmission of bloodborne viruses is unlikely and only HBV, because of the extraordinarily high viral concentration in blood, is thought to have a real potential for such transmission. No epidemiologic or laboratory data support the hypothesis that surgeons or other health care workers are at increased risk of infection by bloodborne pathogens. Although theoretically possible, airborne transmission does not appear likely. Studies that claim to show the potential for airborne transmission of bloodborne pathogens ignore the basic principles of aerobiology and the requirements for proving environmental transmission.
Simulated dialysis of whole blood was used to determine whether membrane factors (biocompatibility), endotoxin (ET) membrane diffusion, or transmembrane monocyte-ET interactions would stimulate tumor necrosis factor (TNF alpha) release. Whole blood containing EDTA and aprotinin was recirculated in the blood compartment of hollow fiber dialyzers containing either regenerated cellulose or polysulfone membranes. ET-free and ET-spiked dialysate were recirculated consecutively in the dialysate compartment for 30 min each. Blood and dialysate samples were collected at to and after each 30 min of simulated dialysis for determination of TNF alpha and ET concentrations. TNF alpha was not detected in any blood samples collected after simulated dialysis with regenerated cellulose (RC) membranes and ET-free or ET-spiked dialysate. However, blood ET concentrations, as determined by the Limulus amebocyte lysate (LAL) assay, increased in RC dialyzers after each 30 min of simulated dialysis even with ET-free dialysate. Since TNF alpha was not detected in these blood samples, the material detected by the LAL assay probably was not ET but an LAL-reactive material. After simulated dialysis with polysulfone dialyzers and ET-free dialysate, TNF alpha and ET were not detected in blood samples. ET also was not detected in blood samples after dialysis with ET-spiked dialysate. However, TNF alpha was detected in 7 of 13 (54%) of the blood samples following the 500 ng/ml of ET dialysate spike. TNF alpha release during simulated dialysis with polysulfone membranes and ET-contaminated dialysate may be due to transmembrane stimulation of circulating mononuclear cells and not diffusion of ET across the membrane.
Endotoxin is a potent activator of the complement system and other host immunoregulators, including the cytokines, tumor necrosis factor alpha, interleukin-1 beta, and interleukin-6. In this study, the potency of an endotoxin from bicarbonate dialysate was compared with endotoxins from two enteric microorganisms, Shigella flexneri and Escherichia coli. Endotoxin concentrations were standardized for the three endotoxins by use of the Limulus amebocyte lysate turbidimetric assay. Endotoxin potency was assessed by the comparative plasma concentrations of tumor necrosis factor alpha, interleukin-1 beta, and interleukin-6 after an in vitro whole-blood challenge by each type of endotoxin. Blood collected from 10 hemodialysis patients was spiked with 0.1, 1, and 10 ng/mL of E. coli and Shigella endotoxin and with 1 and 10 ng/mL of bicarbonate dialysate endotoxin. After incubation, plasma was separated and frozen at -70 degrees C until assayed for cytokine concentrations. Dialysate endotoxin was found to be 10 to 100 times less potent than E. coli and Shigella endotoxins. It was concluded that there are significant differences in the potency of endotoxins from different strains of bacteria and that these differences should be noted when designing or evaluating studies on the clinical effects of endotoxins in hemodialysis settings.
Uremia has been associated with immunologic aberrations, including anergy, increased susceptibility to infections, and reduced phagocytic activity of polymorphonuclear leukocytes. In this study, cytokine release in uremic and nonuremic blood after in vitro endotoxin stimulation was studied. Blood from nonuremic controls, chronic renal failure patients not on dialysis, and chronic hemodialysis patients predialysis and postdialysis was spiked with 10 ng/mL of Escherichia coli endotoxin and incubated for 2 and 26 h. Plasma tumor necrosis factor-alpha (TNF alpha) concentrations were determined by ELISA after each incubation period. To further study which uremic blood component may be responsible for enhanced release of TNF alpha, plasma and cellular components of chronic renal failure patients and controls were switched and then given an in vitro endotoxin stimulation (1 ng/mL). It was found that (1) TNF alpha release is enhanced by uremia and is exacerbated with progressive declines in renal function, (2) enhanced TNF alpha release is related to a blood cellular phenomenon induced by uremia, and (3) enhanced TNF alpha release in hemodialysis patients is associated with a prolonged stimulation and/or reduced plasma elimination of TNF alpha.
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Six common water bacteria were examined for their ability to colonize polyvinyl chloride (PVC) surfaces, survive various germicidal treatment, and re-establish themselves in sterile distilled water (SDW). For each test, two 30.4 cm PVC pipes attached to a 90 degrees PVC elbow were filled with 600 ml of distilled water inoculated with either Pseudomonas aeruginosa, Ps. cepacia, Ps. mesophilica, Acinetobacter anitratus, Mycobacterium chelonae or M. chelonae var. abscessus. After 8 weeks contaminated water was removed and the pipes were exposed to 600 ml of 1:213 iodophor disinfectant (ID), 1:128 phenolic detergent (P), 1:256 quaternary ammonium compound (QA), stock iodophor antiseptic (IA), 2% formaldehyde (F), 10-15 ppm free chlorine (C), 2% glutaraldehyde (G) and 70% ethanol (E). These germicides were periodically sampled, neutralized and examined for surviving organisms. After exposure for 7 d the germicides were removed and each pipe was refilled with SDW. This was assayed at 7 d intervals to determine microbial re-establishment. Samples were removed during microbial conditioning and examined by scanning electron microscopy (SEM). Pseudomonads were isolated directly from ID, QA, C, P and F, and mycobacteria from QA, IA, ID, P, G, C and F. Pseudomonas aeruginosa and Ps. cepacia survived in PVC pipes after 7 d of exposure to P, ID and C; Ps. mesophilica, after C and ID; and both mycobacteria, after C. SEM examination of PVC remnants revealed bacterial attachment and formation of extracellular material with embedded cells. These studies show that common water bacteria can attach and colonize the interior surface of PVC pipes and develop significant resistance to the action of certain germicides.(ABSTRACT TRUNCATED AT 250 WORDS)
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Whole blood and peripheral blood mononuclear cell (PBMC) culture models have been used to study cytokine stimulation and release in vitro. In this study, we characterize the kinetics of the interleukins (IL-1 beta), (IL-6), (IL-8), and tumor necrosis factor-alpha (TNF-alpha) following an endotoxin (ET) challenge using our in vitro whole blood model. Whole blood samples from 10 healthy volunteers were studied. All cytokines were measured by enzyme-linked immunosorbent assay. Peak concentrations of TNF-alpha occurred 2 h after ET challenge followed by a rapid decline in free plasma TNF-alpha concentration (half-life 18.2 min). IL-1 beta was not significantly elevated until 4 h after ET challenge. IL-8 was elevated 1 h after ET challenge. IL-6 concentration exhibited a biphasic peak occurring at 6 and 74 h after ET challenge. We conclude that (1) our whole blood in vitro model produces cytokine release kinetics similar to those reported in vivo, and (2) the presence of either binding proteins or cellular metabolism of TNF-alpha in whole blood produces a similar plasma half-life to that observed in vivo.