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PubMed2004

[The expression of RANTES interleukin 1beta and endotoxin in the effusion of secretory otitis media].

OBJECTIVE: To study the protein expression of endotoxin, interleukin 1beta (IL-1beta) and regulated upon activation, normal T expressed and secreted (RANTES) in effusions of secretory otitis media and their roles in the pathogenesis of secretory otitis media. METHOD: Seventy-two effusion samples were taken from 53 patients with secretory otitis media by tympanocentesis. After swabs they were taken for bacteria culture. Limulus amebocyte lysate (LAL) test was used to quantify the content of endotoxin, radioimmunoassay to analyze the level of IL-1beta and enzyme-linked immunosorbent assay (ELISA) to detect the concentration of RANTES. RESULT: Endotoxin, IL-1beta and RANTES were detectable in 80.9%, 77.8% and 70.8% of middle ear effusion, with mean levels of (35.2 +/- 51.6) EU/ml, (1.10 +/- 0.84) microg/L and (0.52 +/- 0.43) microg/L respectively. All of them showed higher concentration in the mucoid-type effusions than those in the serous-type effusions (P<0.05). Higher levels of the endotoxin and RANTES (P<0.05) were found in longer course patients. The effusions with positive bacteria culture displayed more abundant endotoxin, IL-1beta and RANTES protein than those with negative culture. Significant correlations were found between endotoxin and IL-1beta (r = 0.74, P<0.01), also between IL-1beta and RANTES (r = 0.48, P<0.01). CONCLUSION: Endotoxin, IL-1beta and RANTES may take part in maintaining the inflammatory response in the tympanic cavity and stimulating mucin secretion. It indicates that they play an important role in the immune pathogenesis of secretory otitis media.

Adolescent↗
PubMed1992

Calcitonin gene-related peptide (CGRP) and neuropeptide Y (NPY) levels are elevated in plasma and decreased in vena cava during endotoxin shock in the rat.

Calcitonin gene-related peptide (CGRP), a potent vasodilator, and neuropeptide Y (NPY), a potent vasoconstrictor and potentiator of norepinephrine-induced vasoconstriction, were examined in an animal model of endotoxin shock. Gram-negative bacterial endotoxin (lipopolysaccharide B from Salmonella enteritidis) was administered as a bolus (16.7 mg/kg, i.v.) to conscious, unrestrained rats, previously cannulated for blood pressure measurements and blood withdrawal. At 30 min, endotoxin caused 35-40 mm Hg drop in mean arterial pressure and significant increases in heart rate and plasma levels of glucose and lactate. By 3 hr, blood pressure had returned to near normal levels and remained normal until cardiovascular collapse at 4-6 hr (approximately 70% of the rats). Endotoxin elevated plasma CGRP levels by fourfold at 30 min and 22-fold at 3 hr. Of the organs tested, only vena cava showed significant decreases in CGRP levels. Endotoxin also elevated plasma NPY levels by 67% and decreased NPY levels in adrenal gland and vena cava at 30 min and 3 hr. The data suggest that both CGRP and NPY are released into the circulation during development of endotoxin shock in the rat. NPY may contribute to the compensatory mechanism, tending to bring arterial pressure back to normal levels during intermediate stages of endotoxemia. CGRP, because of its extremely high potency as a hypotensive agent, may contribute to the hypotension at both early and late stages during pathogenesis of endotoxin shock.

Animals↗
PubMed2004

Side-by-side comparison of three sampling methods for aerosolized endotoxin in a wastewater treatment facility.

Research studies have established the occurrence of adverse health effects in individuals exposed to organic dusts and water aerosols laden with endotoxin. To determine what exposure levels cause these health effects, it is necessary to quantify airborne endotoxin. Several scientific studies have demonstrated that the quantification of detectable endotoxin is affected by differences in sampling media, analytical method, and aerosol composition. The study reported here performed side-by-side endotoxin sampling using a liquid impinger, a glass fiber filter, and a polycarbonate filter in a wastewater treatment plant. Results show levels of detected endotoxin appear to be highest with the impinger. Coefficients of variation calculated for each sampling method show the glass fiber filter having the least variability when sampling was conducted at the highest endotoxin levels. Lastly, a Spearman rank order correlation test identified an apparent correlation between endotoxin levels obtained with the impinger and the glass fiber filter.

Aerosols↗
PubMed2005

Effects of endotoxin on serum chemokines in man.

AIM: Endotoxin is known to be a primary initiator of sepsis and septic shock. Migration of immunocompetent cells due to chemotactic attraction plays a central role in the initiation of the immune response. Two major groups of chemokines can be distinguished: C-x-C chemokines like Interleukin-8 attract mainly neutrophils, C-C chemokines (e.g. RANTES) attract monocytes and T-cells. The aim of this study was to get further insight into chemokine profiles after a single endotoxin bolus in man. MATERIALS AND METHODS: We investigated the effect of systemically administered endotoxin (4ng/kg BW i.v.) in 8 healthy volunteers. Clinical data (heart rate, mean arterial pressure, temperature), serum levels of IL-8, and RANTES, as well as white blood cell count were obtained before and hourly for five hours after endotoxin administration. RESULTS: Heart rate and MAP showed significant changes (p<0.05) after 2-3 hours. All volunteers presented with low-grade fever after 2 hours. WBC was elevated 43% and 63% after 4 and 5 hours, respectively. Both chemokines were significantly different from baseline two hours after endotoxin challenge: While IL-8 was significantly increased RANTES serum levels were diminished. CONCLUSION: From our data we conclude that this endotoxin model was effective to mimic the clinical appearance of sepsis. Chemokines like IL-8 and RANTES are integrated in the early immune response to endotoxin challenge in man.

Adult↗
PubMed2006

[Kinetic turbidimetric limulus assay of bacterial endotoxin in the replacement solution of on-line hemodiafiltration].

OBJECTIVE: To determine bacterial endotoxin in the replacement solution of on-line hemodiafiltration (on-line HDF) using kinetic turbidimetric limulus test. METHODS AND RESULTS: Validation test was performed with the replacement solution of on-line HDF in which quantified standard endotoxin was added. The recovery rates of endotoxin from the replacement solution and its dilutions at 1/5, 1/10, and 1/20 were 58.17%, 106.7%, 99.00% and 98.79%, respectively, suggesting that the optimal dilution was at 1/10. Standard endotoxin was added into the replacement solution of on-line HDF of 3 batches (040408, 040511,040527), and the recovery rates in their dilution at 1/10 were 76.32%, 99.00% and 96.24%, respectively. The standard endotoxin in the working curve was 1.00, 0.125, and 0.0156 Eu/ml (endotoxin unit/ml), and the dilution at 1/10 of the replacement solution is effective to eliminate the interference in limulus test. CONCLUSION: Kinetic turbidimetric limulus test provide a means to detect endotoxin in the replacement solution of on-line HDF.

Endotoxins↗
PubMed2006

[Influence on the concentration of plasma endotoxin by inhibition of complement activation in traumatic hemorrhagic shock rats].

OBJECTIVE: To investigate the influence on the concentration of plasma endotoxin by inhibition of complement activation in traumatic hemorrhagic shock rats. METHODS: Eighty male SD rats were randomly divided into two groups: control and cobra venom factor (CVF) treatment groups. The hemorrhagic shock induced by trauma was replicated in both groups. The animals were killed preshock and at 1, 6, and 24 hours postresuscitation. Twenty-four hours before hemorrhage, rats were given a mainline dose of either 50 microg/kg CVF or an equal volume of saline solution. The plasma and serum samples were collected at each time point to determine the concentration of endotoxin, the activity of CH50 and diamine oxidase (DAO), and the level of tumor necrosis factor (TNF-alpha) at various time points in two groups. RESULTS: Compared with preshock in control group, serum CH50 levels were decreased promptly at 1 hour postresuscitation. Markedly elevation of the levels of endotoxin and TNF-alpha in blood were found at early time after resuscitation, and they were come rapidly back to the basic level at 6 and 24 hours phase. The activity of DAO in blood was increased significantly at 1 and 6 hours after resuscitation and declined promptly at 24 hours. Compared with the control group, significantly decline of the levels of endotoxin, TNF-alpha and DAO at the various time points after resuscitation were also found in the CVF group. The levels of CH50 in CVF group were always less than 5% during the experiment. CONCLUSION: In traumatic hemorrhagic shock rats CVF pretreatment could decline plasma endotoxin levels by preventing the injury of intestine and gut barrier function, decrease endotoxin translocation and reduce plasma endotoxin levels.

Animals↗
PubMed1991

Endotoxin stimulates bronchial epithelial cells to release chemotactic factors for neutrophils. A potential mechanism for neutrophil recruitment, cytotoxicity, and inhibition of proliferation in bronchial inflammation.

To test the effect of endotoxin on bronchial epithelial cells (BEC), BEC were isolated from bovine lungs and cultured in the presence of bacterial endotoxin. The BEC culture supernatant fluids were harvested, and neutrophil chemotactic activity (NCA) was determined with a blindwell chamber technique; cytotoxicity determined by lactate dehydrogenase release and BEC proliferation determined by Coulter counting. Endotoxin caused a dose- and time-dependent release of NCA from BEC cultures compared with media alone (82.3 +/- 8.1 vs 12.0 +/- 3.1 cells/high power field, p less than 0.001). To further characterize this activity, reverse phase HPLC analysis of release eicosanoid metabolites after [3H]arachidonic acid incorporation was performed. Endotoxin stimulated the release of the neutrophil chemoattractants, leukotriene B4 and 12-hydroxyeicosatetraenoic acids. Endotoxin also resulted in a dose and time dependent release of lactate dehydrogenase (42.9 +/- 4.2 vs 20.2 +/- 2.2 U/liter, p less than 0.001) although higher doses were required to cause cytotoxicity than to stimulate chemotaxis. Finally, endotoxin resulted in a dose dependent inhibition of BEC proliferation (176 x 10(3) +/- 16 x 10(3) vs 1,080 x 10(3) +/- 38 x 10(3) cells/ml measured at day 14, p less than 0.001). These data suggest that bacterial release of endotoxin may contribute to the pathophysiologic changes observed in bronchial inflammation by stimulating BEC to release NCA, denuding airway epithelium by causing cytotoxicity of BEC, and inhibiting epithelial repair by inhibiting BEC proliferation.

Animals↗
PubMedDate not supplied

Endotoxemia is masked in fungal infection due to enhanced endotoxin clearance by beta-glucan.

Employing a novel turbidimetric assay, the amount of endotoxin and beta-glucan in plasma was monitored in postoperative patients suffering from both bacterial and fungal infections. The patients, whose beta-glucan level was markedly elevated, were always negative for endotoxin, suggesting a possible role of beta-glucan in the clearance of circulating endotoxin. In order to test the above hypothesis, effects of beta-glucan (carboxy methylated curdlan or lentinan) on endotoxin clearance were studied in rabbits. beta-glucan (4 micrograms/kg or 40 micrograms/kg) was intravenously administered to rabbits which received 4 micrograms/kg endotoxin injection, simultaneously or 120 min before the injection. Either of the beta-glucans increased the endotoxin clearance in a dose-dependent manner, and the preinjection of beta-glucan was more effective than the coinjection. The increased amount of plasma beta-glucan results in the unexpectedly low level of plasma endotoxin, which may be removed by the reticuloendothelial system activated by beta-glucan, in cases with both bacterial and fungal infections. Thus, it is important to recognize that endotoxemia may be masked by the coexisting fungal infection.

Adjuvants, Immunologic↗
PubMed1991

Electron microscopic study of the effects of endotoxin on the cells of the hepatic sinusoid in normal and BCG sensitized mice.

Electron microscopic studies were conducted to access ultrastructural alterations in Kupffer cells and other cells lining the hepatic sinusoids at the peak of mediator release two hours after challenge with low doses of endotoxin under various conditions including reticuloendothelial system (RES) expansion and activation with BCG. BCG is known to sensitize animals to endotoxin rendering normally innocuous, low doses of endotoxin lethal. Low non-lethal doses (5 micrograms) of endotoxin activated Kupffer cells as well as caused isolated foci of cellular injury. However, animals which were treated with BCG had a highly activated and expanded RES system as evidenced by enlarged Kupffer cells with many extended cellular processes. Granulomas were prevalent and many reactive cells were present. After two hours marked cellular injury occurred to sinusoid lining and parenchymal cells when BCG treated animals were challenged with these same low doses of endotoxin. Cellular debris, fibrin, and platelets were observed in sinusoids often associated with Kupffer cells. These results suggest that the functional state of Kupffer cells is an important determinant in the host response to endotoxin. While there appears to be an effective clearance of endotoxin; the release of mediators by the highly activated Kupffer cells can be toxic causing hepatocellular injury.

Animals↗
PubMed1991

Effects of flunixin meglumine on endotoxin-induced prostaglandin F2 alpha secretion during early pregnancy in mares.

The role of prostaglandin F2 alpha (PGF2 alpha) in embryonic loss following induced endotoxemia was studied in mares that were 21 to 44 days pregnant. Thirteen pregnant mares were treated with a nonsteroidal anti-inflammatory drug, flunixin meglumine, to inhibit the synthesis of PGF2 alpha caused by Salmonella typhimurium endotoxin given IV. Flunixin meglumine was administered either before injection of the endotoxin (group 1, -10 min; n = 7), or after endotoxin injection into the mares (group 2, 1 hour, n = 3; group 3, 2 hours, n = 3); 12 pregnant mares (group 4) were given only S typhimurium endotoxin. In group 4, the secretion of PGF2 alpha, as determined by plasma 15-keto-13,14-dihydro-PGF2 alpha concentrations, was biphasic, initially peaking at 30 minutes followed by a second, larger peak approximately 105 minutes after the endotoxin was given IV. When flunixin meglumine was administered at -10 minutes, synthesis of PGF2 alpha was inhibited for several hours, after administration of flunixin meglumine at 1 hour, the second secretory surge of PGF2 alpha was blocked, and administration of the drug at 2 hours did not substantially modify the secretion of PGF2 alpha. Plasma progesterone concentrations were unchanged after endotoxin injections were given in group 1. In group 2, progesterone values decreased less than 2 ng/ml and remained low for several days. In group 3 and group 4, progesterone concentrations decreased to values less than 0.5 ng/ml by 48 hours after endotoxin injections were given.(ABSTRACT TRUNCATED AT 250 WORDS)

Abortion, Veterinary↗
PubMed1990

[Methodological and clinical evaluation of a microplate assay of endotoxin in whole blood sample].

We have developed a simple, rapid method for determining endotoxin in whole blood using a microtiter plate. The samples were pretreated with 0.66 mol/l nitric acid containing 0.25% Triton X-100; the supernatants were placed in a microtiter plate well, and incubated with endotoxin-specific chromogenic limulus test reagent (Endospecy; Seikagaku Corporation). The calibration curve was linear from 0 to 50 pg/ml of Escherichia coli 0111: B4 endotoxin with a variation coefficient less than 5%. The recovery of endotoxin added to human and experimental animals was about 100% without being affected by dilution. The normal endotoxin level in human whole blood was less than 10 pg/ml in reference to E. coli 0111: B4 endotoxin. The results in 120 patients with various diseases correlated well with those determined by a conventional method using plasma as a sample (r = 0.877; p less than 0.05). Whole blood sample has advantages over plasma in that it allows all endotoxin in a sample to be determined, requires a smaller amount of sample, and has less risk of contamination.

Animals↗
PubMed1990

Tumor necrosis factor (TNF) and endotoxin prime effects of PAF in vivo.

The purpose of the present study in NMRI mice was to investigate the action of platelet-activating factor (PAF) on mortality and intestinal transit velocity, the interaction of endotoxin or tumor necrosis factor (TNF) with the effect of PAF on these parameters and the effect of the PAF antagonist WEB 2086 on the endotoxin/TNF- and PAF-induced changes. PAF at a high dose (200 micrograms/kg i.v.) increased mortality and reduced transit velocity. This effect was inhibited by WEB 2086 (0.01-0.5 mg/kg i.p.) in a dose-dependent manner. Pretreatment with endotoxin (S. typhosa; 10 micrograms/kg i.v.) or TNF (40 micrograms/kg i.v.) enhanced the activity of PAF resulting in increased mortality and reduced transit velocity. This enhanced activity of PAF in the case of pretreatment with endotoxin or TNF occurred at doses at which PAF, endotoxin or TNF given alone did not significantly affect these parameters. The ability of endotoxin or TNF to enhance the effect of PAF was maximal, if the time delay between endotoxin and subsequent PAF administration was about 1-2 h. WEB 2086 (0.01-1 mg/kg i.p.) inhibited this priming in a dose-dependent fashion. These findings support suggestions of a role for PAF in endotoxin shock and TNF-associated shock-like syndrome.

Animals↗
PubMed1990

Mechanisms of myocardial membrane alterations in endotoxin shock: roles of phospholipase and phosphorylation.

Current progress in the studies of myocardial membrane alterations during endotoxin shock indicates that endotoxin administration impairs (Na(+) + K(+)-ATPase enzyme system by disrupting the coordination of the ouabain receptor subunit and the catalytic subunit of the enzyme system, and that the disruption is due to an alteration in the lipid microenvironment and a decrease in the phosphorylated intermediate of the enzyme cycle. Studies of the membrane lipid profile provide evidence that endotoxin administration modifies the molecular structure of cardiac membrane lipids in association with the activation of phospholipases A1 and A2 and with the inhibition of phospholipid methylating enzymes. Using liposomes as a membrane model for investigation, endotoxin was found to be capable of modifying the physical property of membrane phospholipids by altering the molecular packing and the phase transition temperature of lipid bilayers. Further studies with Na(+)-Ca2+ exchange system in cardiac sarcolemma have established the roles of phospholipase A2 and protein phosphorylation on the endotoxin-induced derangement in myocardial Na(+)-Ca2+ exchange. Based on these studies, it is concluded that endotoxin administration exerts multiple injuries in different membrane-associated enzyme/receptor systems and that the mechanisms responsible for the endotoxin-induced membrane damage can be categorized into two conceptual frameworks: namely, changes in membrane lipid microenvironment in response to phospholipase A activation and alterations in the phosphorylation of the enzyme/receptor proteins.

Animals↗
PubMed1990

Endotoxin-induced tumor necrosis factor activity production by equine peritoneal macrophages.

A study was performed to determine whether equine macrophages produce tumor necrosis factor (TNF) activity in vitro in response to endotoxin and to study the effects of endotoxin concentration and incubation time on the amount of TNF produced. Equine peritoneal macrophages were isolated and cultured in vitro for 2, 6, 12, or 24 hr in tissue culture media containing 1) no additive (nonstimulated control), 2) endotoxin (0.5 ng/ml, 5 ng/ml, or 5 micrograms/ml), or 3) the calcium ionophore A23187 (0.95 microM). The supernatant media concentrations of TNF activity were determined by an in vitro cytotoxicity bioassay using the murine fibrosarcoma cell line WEHI 164 clone 13. At all incubation times, macrophages exposed to endotoxin produced significantly more TNF than did nonstimulated control cells (P less than 0.05). Among the three doses of endotoxin tested, there were no differences in concentrations of TNF activity in the supernatant media. The mean concentration of TNF activity in media from nonstimulated macrophages was significantly less after 24 hr incubation than after 2, 6 or 12 hr. Incubation time had no effect on TNF production by macrophages exposed to 0.5 ng/ml and 5 micrograms/ml endotoxin, but macrophages exposed to 5 ng/ml endotoxin produced significantly more TNF after 6 and 12 hr than after 2 hr. To address the reason for the decrease in TNF activity in media from nonstimulated macrophages over time, a second study was designed to determine the effect of incubation on the activity of TNF under tissue culture conditions. Human recombinant TNF was added to media that was incubated 2-24 hr.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Resistance of essential fatty acid-deficient rats to endotoxin-induced increases in vascular permeability.

Resistance to endotoxin in essential fatty acid-deficient (EFAD) rats is associated with reduced synthesis of certain arachidonic acid metabolites. It was hypothesized that EFAD rats would manifest decreased vascular permeability changes during endotoxemia as a consequence of reduced arachidonic acid metabolism. To test this hypothesis, changes in hematocrit (HCT) and mesenteric localization rate of technetium-labeled human serum albumin (99mTc-HSA) and red blood cells (99mTc-RBC) were assessed in EFAD and normal rats using gamma-camera imaging. Thirty minutes after Salmonella enteritidis endotoxin, EFAD rats exhibited less hemoconcentration as determined by % HCT than normal rats (47 +/- 2% vs. 54 +/- 1% respectively, P less than 0.01). Endotoxin caused a less severe change in permeability index in the splanchnic region in EFAD rats than in normal rats (1.2 +/- 0.6 x 10(-3)min-1 vs. 4.9 +/- 1.7 x 10(-3)min-1 respectively, P less than 0.05). In contrast to 99mTc-HSA, mesenteric localization of 99mTc-RBC was not changed by endotoxin in control or EFAD rats. Supplementation with ethyl-arachidonic acid did not enhance susceptibility of EFAD rats to endotoxin-induced splanchnic permeability to 99mTc-HSA. Leukotrienes have been implicated as mediators of increased vascular permeability in endotoxin shock. Since LTC3 formation has been reported to be increased in EFA deficiency, we hypothesized that LTC3 may be less potent than LTC4. Thus the effect of LTC3 on mean arterial pressure and permeability was compared to LTC4 in normal rats. LTC3-induced increases in peak mean arterial pressure were less than LTC4 at 10 micrograms/kg (39 +/- 5 mm Hg vs. 58 +/- 4 mm Hg respectively, P less than 0.05) and at 20 micrograms/kg (56 +/- 4 mm Hg vs. 75 +/- 2 mm Hg respectively, P less than 0.05). LY171883 (30 mg/kg), an LTD4/E4 receptor antagonist, attenuated the pressor effect of LTC4, LTD4, and LTC3. Infusion of LTC4 (4 micrograms/kg/min) in normal rats induced a rise in HCT from 44 +/- 1% to 51 +/- 1% (P less than 0.01), which was greater (P less than 0.05) than the rise induced by LTC3 (47 +/- 1% to 49 +/- 1%). The results showing that EFAD rats are resistant to endotoxin-induced increases in HCT and vascular permeability raise the possibility that this may, in part, be a result of preferential LTC3 production that is less potent than LTC4.

Animals↗
PubMed1990

Protection against endotoxin-induced foetal resorption in mice by desferrioxamine and ebselen.

Endotoxin was administered to mice on their 13th day of pregnancy at doses which caused the resorption of approximately 50% of the implanted foetuses. The iron chelator desferrioxamine was found to significantly inhibit the percentage of resorptions induced by endotoxin in a dose-dependent manner. The highest dose of desferrioxamine (5 mg) given intravenously 30 min prior to, immediately after, and 4 and 24 h after endotoxin inoculation, reduced the percentage of resorptions from 56.9 to 17.9%. Administration of the novel selenium-containing compound ebselen, which is both an antioxidant and an inhibitor of leukotriene synthesis, was also found to significantly protect against endotoxin-induced foetal resorptions, reducing the percentage of resorbed foetuses from 52.9 to 26.0% when given at a dose of 50 mg/kg (s.c.) at the time of endotoxin inoculation and 24 and 48 h following. Both these compounds also significantly reduced the increase in spleen weights observed when the mice were given endotoxin. These results provide evidence that the iron-catalysed production of hydroxyl radicals from other oxygen-derived species and the formation of leukotrienes play an important role in the mechanism by which endotoxin causes foetal resorptions in the mouse.

Animals↗
PubMedDate not supplied

Backdiffusion rather than backfiltration enhances endotoxin transport through highly permeable dialysis membranes.

Endotoxin transfer from dialysate to blood by backfiltration has been reported to occur when highly permeable dialysis membranes available for efficient removal of beta-2-microglobulin are used clinically. Little is known concerning endotoxin transfer from dialysate to blood by diffusion. The present paper describes technical determination of diffusive and convective clearances for endotoxins based on conventional mass and momentum transfer models. Fractional diffusive transport of endotoxins with molecular weights of 1,000 and 10,000 daltons approximated unity. This indicates that clean-up of contaminated dialysate is necessary for safe hemodialysis treatment with highly permeable dialysis membranes. Diffusive in-flow of endotoxin with a molecular weight of 1,000 was calculated to be 278 and 88 pg/min for PAN-12CX2 and MC0.8H at an endotoxin concentration of inflowing dialysate of 2 pg/ml. These results demonstrate that dialysate should be carefully cleaned to prevent diffusive inflow of endotoxins from dialysate to blood.

Blood Flow Velocity↗
PubMed1990

Endotoxin and bacterial contamination of dialysis center water and dialysate; a cross sectional survey.

The bacterial and endotoxin levels of purified water and effluent dialysate were examined in a cross section of dialysis centers in the central United States. All samples were collected within a four-hour drive of the University of Louisville and were collected, processed and analyzed by our personnel, to eliminate variability in sample handling. A medium capable of higher bacteria recovery from aqueous environments than those ordinarily employed in clinical assays was used. Endotoxins were determined by a quantitative colorimetric assay. By the more sensitive bacterial assay 53% of the centers had bacterial counts above the AAMI standard of 200 colony-forming units per ml (CFU/ml) for water and 35% of the centers had bacterial counts above the 2000 CFU/ml standard for dialysate in at least one sampling period. The samples showed 35% and 19% of water and dialysate above the standards, respectively. While there are no standards for endotoxin concentrations in water used to prepare dialysate, 2% of the centers had endotoxin levels in their water above five endotoxin units per ml (5 EU/ml = 1 ng/ml in our assay kit), the limit set by the AAMI standards for reprocessor water. Both bacterial and endotoxin levels tended to be elevated in dialysate, with the highest levels of endotoxin in dialysates posing an obvious potential risk when high-flux dialyzers are used.

Bacteria↗