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P Bailly

Publications and source records attributed to P Bailly.

At least 19 recordsLinked to original sources

Results from a four-year study on the prevalence of nosocomial infections in Franche-Comté: attempt to rank the risk of nosocomial infection.

The aim of this study was to rank the risk of nosocomial infection (NI) according to patient type by analysing the results of annual prevalence studies carried out in Franche-Comté from 2001 to 2004. Patients (N=14,905) were divided into four categories according to the number of endogenous risk factors (age, immunodepression, MacCabe score). The overall prevalence of infection was 6.1% and varied according to the category of patient from 1.93% (no risk factors) to 15.2% (three risk factors). The frequencies of NI related to an invasive procedure and to cross-contamination with multi-drug-resistant (MDR) bacteria were 30.9% and 12.3%, respectively; these percentages did not depend on the type of patient. The prevalence of NI decreased over time for patients with two or three risk factors, but was stable for patients with no risk factors. More than 40% of NIs were potentially avoidable (related to invasive procedures or involving cross-transmission of an MDR bacterium) regardless of the category of patient. This study suggests that at least 30% of NIs could be avoided.

Age Factors↗

[Influenza vaccination among health-care workers. Vaccination rates in universitary hospital of Besançon, winter 2003-2004].

BACKGROUND: Influenza vaccination reduces the mortality of the patients when the vaccination rates of healthcare workers is important. PURPOSE AND METHOD OF THE STUDY: To investigate the vaccination rates at the Universitary Hospital of Besançon by anonymous questionnaire. RESULTS: Three thousand hundred seventy-seven answers were analyzed (228 men and 1145 women). Two hundred seventy-seven persons declared receiving the vaccine (20.1%) corresponding to sixty-three men (27.6%) and two hundred thirteen women (18.6%) (P = 0.001). The average age of the healthcare workers vaccined was of 38.9+/-11 years. Among most than 50 years, 34% was vaccined. Among the doctors, 40.5% were vaccined against 20.6% of the nurses. In the services of geriatrics, 78.5% of the staff was vaccined. CONCLUSIONS: Our results indicate a weak rate of influenza vaccination in our establishment and a misunderstanding of the character nosocomial of the influenza among the nurse.

France↗

[Methicillin-resistant Staphylococcus aureus (MRSA) in rehabilitation and chronic-care-facilities: what is the best strategy?].

BACKGROUND: The risk associated with methicillin-resistant Staphylococcus aureus (MRSA) has been decreasing for several years in intensive care departments, but is now increasing in rehabilitation and chronic-care-facilities (R-CCF). The aim of this study was to use published data and our own experience to discuss the roles of screening for MRSA carriers, the type of isolation to be implemented and the efficiency of chemical decontamination. DISCUSSION: Screening identifies over 90% of patients colonized with MRSA upon admission to R-CCF versus only 50% for intensive care units. Only totally dependent patients acquire MRSA. Thus, strict geographical isolation, as opposed to "social reinsertion", is clearly of no value. However, this should not lead to the abandoning of isolation, which remains essential during the administration of care. The use of chemicals to decolonize the nose and healthy skin appeared to be of some value and the application of this procedure could make technical isolation unnecessary in a non-negligible proportion of cases. SUMMARY: Given the increase in morbidity associated with MRSA observed in numerous hospitals, the emergence of a community-acquired disease associated with these strains and the evolution of glycopeptide-resistant strains, the voluntary application of a strategy combining screening, technical isolation and chemical decolonization in R-CCF appears to be an urgent matter of priority.

Carrier State↗

UT-B1 urea transporter is expressed along the urinary and gastrointestinal tracts of the mouse.

Selective transporters account for rapid urea transport across plasma membranes of several cell types. UT-B1 urea transporter is widely distributed in rat and human tissues. Because mice exhibit high urea turnover and are the preferred species for gene engineering, we have delineated UT-B1 tissue expression in murine tissues. A cDNA was cloned from BALB/c mouse kidney, encoding a polypeptide that differed from C57BL/6 mouse UT-B1 by one residue (Val-8-Ala). UT-B1 mRNA was detected by RT-PCR in brain, kidney, bladder, testis, lung, spleen, and digestive tract (liver, stomach, jejunum, colon). Northern blotting revealed seven UT-B1 transcripts in mouse tissues. Immunoblots identified a nonglycosylated UT-B1 protein of 29 kDa in most tissues and of 36 and 32 kDa in testis and liver, respectively. UT-B1 protein of gastrointestinal tract did not undergo N-glycosylation. Immunohistochemistry and in situ hybridization localized UT-B1 in urinary tract urothelium (papillary surface, ureter, bladder, and urethra), prominently on plasma membranes and restricted to the basolateral area in umbrella cells. UT-B1 was found in endothelial cells of descending vasa recta in kidney medulla and in astrocyte processes in brain. Dehydration induced by water deprivation for 2 days caused a tissue-specific decrease in UT-B1 abundance in the urinary bladder and the ureter.

Animals↗

[Hospital deaths attributable to nosocomial infections: surveillance in a university hospital].

OBJECTIVE: A system for monitoring deaths was set up at the Besançon University Hospital, in the Franche-Comté region of France, in January 2002. This article describes the principal results after 1 year of activity. MATERIALS AND METHODS: The main outcome was the descriptive surveillance of deaths due to nosocomial infections (NI), by means of a two-step process, in the identification of cases. The first step was the declaration of information concerning the possible existence of an NI at the time of death and the assignment of a prognostic score to each patient upon admission. The second step involved comparison of opinions concerning cases "selected" on the basis of clinical records. This system was completed by a methodological analysis of deaths considered to be partially or totally due to NIs, with the aim to suggest preventive actions. RESULTS: The overall rate of mortality in our hospital was 2.44 per 100 patients admitted. The overall proportion of deaths linked to hospital-acquired infections was 15.3%. We analysed eight of the 20 deaths possibly due to NI (MacCabe score of 1 or 0) in detail. In three of these eight cases, we showed that the cause of death was not NI. Methodical analysis of patient records showed that corrective actions could have been taken in three of these five cases. CONCLUSION: Our study suggests that it is possible to monitor deaths due to nosocomial infections continuously in a university hospital and favours re-implementing death analysis committees acknowledging the "useful error" concept which is culturally difficult to accept.

Adolescent↗

[Determination of indicators for non-compliance with guidelines for surgical antimicrobial prophylaxis].

We conducted a prospective study to identify predictors of inappropriateness of surgical prophylaxis. A total of 72 surgeon-anaesthesist pairs participated in data collection. We assessed practices by addressing 5 questions: did the surgical procedure justify the use of antimicrobial prophylaxis, and was it provided? Was the correct agent used? Was the timing of prophylaxis optimal? Was the duration of prophylaxis correct? Was the dose correct? We reviewed 687 procedures, 513 (74.7%) of which were included in the analysis. The proportion of these procedures with totally compliant prescriptions was 41.7%. Of the 156 patients who received an inappropriate drug, 133 (85.3%) received a drug with a broader spectrum than that recommended. Prophylaxis lasted too long in 81 (89.0%) of the 91 patients who received prophylaxis of incorrect duration. Multivariate analysis revealed a clear association between non-compliant prophylaxis and two operation-specific factors: prosthesis implantation (with a relative risk of 2.52) and clean-contaminated operations (with a relative risk of 4.19). More than 50% of patients received inappropriate surgical prophylaxis. Non-observance of guidelines was related to factors that did not influence the infectious potential of the flora.

Adult↗

Non-observance of guidelines for surgical antimicrobial prophylaxis and surgical-site infections.

OBJECTIVE: A prospective multicentre study was conducted to assess major aspects of surgical prophylaxis and to determine whether inappropriate antimicrobial prophylaxis was a factor associated (risk or protective factor) with surgical site infection (SSI). METHOD: Surgical prophylaxis practices were assessed by analysing four variables: indication, antimicrobial agent, timing and duration. Univariate and multivariate analyses were carried out to identify predictors of SSI among patient-specific, operation-specific and antimicrobial prophylaxis-specific factors. RESULTS: The frequency of SSI was 2.7% (13 SSI in 474 observations). Total compliance of the prescription with guidelines was observed in 41.1% of cases (195 prescriptions). Of the 139 patients who received an inappropriate drug, 126 (90.6%) received a drug with a broader spectrum than the recommended drug. Prophylaxis was prolonged in 71 (87.7%) of the 81 patients who received prophylaxis for inappropriate lengths of time and 43 (61.4%) of the 70 patients who did not receive prophylaxis at the optimal moment were treated too late. Multivariate analysis clearly demonstrated that SSI was associated with multiple procedures (relative risk 8.5), short duration of prophylaxis (relative risk 12.7) and long-term therapy with antimicrobial agents during the previous year (relative risk 8.8). CONCLUSIONS: The ecological risk of the emergence of resistance associated with the frequent use of broad-spectrum antibiotics and prophylaxis for longer periods was not offset by individual benefit to the patients who received inappropriate prophylaxis.

Adult↗

UT-B1 proteins in rat: tissue distribution and regulation by antidiuretic hormone in kidney.

UT-B1 is the facilitated urea transporter of red blood cells (RBCs) and endothelial cells of descending vasa recta in the kidney. Immunoblotting with a polyclonal antibody against the C-ter sequence of rat UT-B1 revealed UT-B1 as both nonglycosylated (29 kDa) and N-glycosylated (47.5 and 33 kDa) proteins in RBC membranes, kidney medulla, brain, and bladder in rat. In testis, UT-B1 was expressed only as a nonglycosylated protein of 47.5 kDa. Immunocytochemistry confirmed that the location of UT-B1 is restricted to descending vasa recta. In brain, UT-B1 protein was found in astrocytes and ependymal cells. Cell bodies and perivascular end feet of astrocytes were labeled in brain cortex, whereas astrocyte cell processes were labeled in corpus callosum. Flow cytometry analysis of RBCs revealed a good cross-reactivity of the antibody with mouse and human UT-B1. UT-B1 protein expression in rat kidney medulla was downregulated greatly by long-term [deamino-Cys(1),D-Arg(8)]vasopressin infusion and moderately by furosemide treatment. This study discloses an uneven distribution of UT-B1 protein within astrocytes and the regulation of renal UT-B1 protein by antidiuretic hormone.

Amino Acid Sequence↗

Mitral and mitro-aortic valve replacement with Sorin Bicarbon valves compared with St. Jude Medical valves.

OBJECTIVE: We assessed the clinical results of two bileaflet mechanical valves: the St. Jude Medical (SJM) and the Sorin Bicarbon (Sorin Bicarbon) used either in single mitral valve replacement (MVR) or in double, aortic and mitral, valve replacement (DVR). METHODS: Between September 1990 and November 1995, 217 patients received either a St. Jude Medical (n=134) or a Sorin Bicarbon (n=86): 136 mitral valve replacement with 83 St. Jude Medical and 53 Sorin Bicarbon and 84 double valve replacement with 51 St. Jude Medical and 33 Sorin Bicarbon. There was no difference between both St. Jude Medical and Sorin Bicarbon cohorts in respect of mitral valve physiopathology, etiology of valve disease, associated lesions, echocardiographic and hemodynamic data. The only significant preoperative difference was the age of patients within the double valve replacement group and the size of implanted valves within the mitral valve replacement group. Follow-up was 100% complete with a mean of 39+/-18 months, ranging between 6 and 68 months. The total follow-up was 657 patient-years (pt-y): 396 pt-y in the mitral valve replacement group and 274 pt-y in the double valve replacement group. RESULTS: Hospital mortality (St. Jude Medical: 2.2%; Sorin Bicarbon: 6.9%) and late mortality (St. Jude Medical: 8.4%; Sorin Bicarbon: 6.3%) were not significantly different. Ten deaths were considered valve-related (St. Jude Medical 6, Sorin Bicarbon 4). The estimated 4-yr overall survival, including hospital mortality, was for St. Jude Medical--mitral valve replacement: 89+/-4% and St. Jude Medical--double valve replacement: 93+/-4%, and for Sorin Bicarbon--mitral valve replacement: 87+/-5% and Sorin Bicarbon--double valve replacement: 91+/-5%. The linearized incidence (% per pt-y) of valve-related complications was 6.39 in the St. Jude Medical cohort and 9.2 in the Sorin Bicarbon cohort. The linearized incidence (% pt-y) of the prevalent complication, valve thromboembolism and bleeding, was for St. Jude Medical-mitral valve replacement: 3.41, St. Jude Medical--double valve replacement: 3.16 and for Sorin Bicarbon--mitral valve replacement: 2.17 and Sorin Bicarbon--double valve replacement: 3.67. The differences between each group of an estimated 4-yr freedom from combined thromboembolism and bleeding were not significant (St. Jude Medical--mitral valve replacement: 90+/-4%, St. Jude Medical--double valve replacement: 84+/-6%, and for Sorin Bicarbon--mitral valve replacement: 94+/-3% and Sorin Bicarbon--double valve replacement: 75+/-17%). CONCLUSIONS: In this clinical non-randomized study, there was no evidence of any significant difference between St. Jude Medical and Sorin Bicarbon valves over a 4-yr follow-up.

Actuarial Analysis↗

Multicentre study on the appropriateness of surgical antibiotic prophylaxis.

A prospective study was conducted to assess the appropriateness of surgical antibiotic prophylaxis. A total of 72 surgeon-anaesthesist pairs participated in data collection, which assessed five variables: did the surgical procedure justify the use of antimicrobial prophylaxis and was it given? was an appropriate agent used?, is the timing of administration optimal?, is the duration of prophylaxis correct?, and is a proper dose given? Of the 687 procedures reviewed, 513 (74.7%) were entered in the analysis. Of these procedures, the rate of totally compliant prescriptions was 41.7%. Among the 117 patients who received an inappropriate drug, 112 (95.7%) received a drug with a broader spectrum of activity than that recommended. Prolonged prophylaxis occurred in 80 (87.9%) of the 91 patients who received prophylaxis with an incorrect duration. In conclusion, compliance with the principles of prophylactic antimicrobial administration should be strictly reviewed and conducting such audits should be part of the routine activity of infection control teams.

Antibiotic Prophylaxis↗

Large outbreak in a surgical intensive care unit of colonization or infection with Pseudomonas aeruginosa that overexpressed an active efflux pump.

During a 30-month survey, 55 patients were colonized or infected by a single clone of Pseudomonas aeruginosa in a surgical intensive care unit (ICU). This clone overexpressed an efflux pump system, and its antibiotic resistance pattern was extremely stable as it spread from patient to patient. Pulsed-field gel electrophoresis showed that isolates from different patients were genetically identical or very similar. We were unable to identify an environmental reservoir, but cultures of hand specimens from 2 health care workers were positive. It was not clear whether this carriage was the source of the epidemic or a consequence of it. However, the propagation of the epidemic clone was probably linked to its transmission by the staff from patient to patient. The outbreak was controlled, with difficulty, by strengthening isolation procedures, replacing the antiseptic soap being used by the staff, and changing the antibiotic prescription policy. This observation emphasizes the importance of compliance with hand washing and universal precautions.

Anti-Bacterial Agents↗

Binding sites of leukocyte beta 2 integrins (LFA-1, Mac-1) on the human ICAM-4/LW blood group protein.

The red cell ICAM-4/LW blood group glycoprotein, which belongs to the family of intercellular adhesion molecules (ICAMs), has been reported to interact with CD11a/CD18 (LFA-1) and CD11b/CD18 (Mac-1) beta(2) integrins. To better define the basis of the ICAM-4/beta(2) integrin interaction, we have generated wild-type, domain-deleted and mutated recombinant chimeric ICAM-4-Fc proteins and analyzed their interaction in a cellular adhesion assay with LFA-1 and Mac-1 L-cell stable transfectants. We found that monoclonal antibodies against CD11a, CD11b, CD18, or LW(ab) block adhesion of transfectant L-cells to immobilized ICAM-4-Fc protein and that the ICAM-4/beta(2) integrin interaction was highly sensitive to the presence of the divalent cations Ca(2+) and Mg(2+). Deletion of individual Ig-domains D1 or D2 of the extracellular part of ICAM-4 showed that LFA-1 binds to the first Ig-like domain, whereas the Mac-1 binding site encompassed both the first and the second Ig-like domains. Based on the crystal structure of ICAM-2, we propose a model for the Ig-like domains D1 and D2 of ICAM-4. Accordingly, by site-directed mutagenesis of 22 amino acid positions spread out on all faces of the ICAM-4 molecule, we identified four exposed residues, Leu(80), Trp(93), and Arg(97) on the CFG face and Trp(77) on the E-F loop of domain D1 that may contact LFA-1 as part of the binding site. However, the single and double mutants R52E and T91Q on the CFG face of domain D1, which correspond to the key residues Glu(34) and Gln(73) for ICAM-1 binding to LFA-1, had no effect on LFA-1 binding. In contrast, all mutants on the CFG face of domain D1 and residues Glu(151) and Thr(154) in the C'-E loop of the domain D2 seem to play a dominant role in Mac-1 binding. These data suggest that the binding site for LFA-1 on ICAM-4 overlaps but is distinct from the Mac-1 binding site.

Amino Acid Sequence↗

Molecular heterogeneity of the Jk(null) phenotype: expression analysis of the Jk(S291P) mutation found in Finns.

Polymerase chain reaction genotyping of 32 unrelated Jk(null) individuals originating predominantly from Polynesia and Finland indicated that all were homozygous for the JK*B polymorphism and that 17 of 32, including the 14 Polynesians, carried a 3'-acceptor splice site mutation of intron 5 that resulted in the skipping of exon 6 (called mutation Jk delta 6). The remaining 15 Jk(null) donors from Finland were homozygous for a new T871C transition resulting in a S291P amino acid substitution at a consensus N-glycosylation site of the Jk polypeptide. Transcription-translation assays revealed that the Jk(S291P) mutant was translated into a glycosylated component as efficiently as the wild-type Jk polypeptide (wt Jk)] in the presence of microsomes, thus indicating that the S291P mutation has no effect on the N-glycosylation pattern of the Jk protein. Expression studies in Xenopus oocytes revealed that the Jk(S291P) polypeptide functions as a urea transporter, but the transport activity and the membrane expression level of the mutant protein was reduced to a similar extent. A substantial fraction of the mutant protein was retained intracellularly suggesting that the transit to the plasma membrane was reduced, presumably because of the S-->P mutation. After transfection in erythroleukemia K562 cells the wild-type, but not the mutant, protein was efficiently expressed at the cell surface. Because the Jk(S291P) mutant polypeptide was not present in human red cells from Jk(null) individuals, expression data in the erythroid context clearly indicates that the S-->P mutation is the molecular basis of the Finnish Jk(null) phenotype. (Blood. 2000;96:1566-1573)

Finland↗

Clinical and molecular epidemiology of chromosome-mediated resistance to third-generation cephalosporins in Enterobacter isolates in eastern France.

OBJECTIVE: To determine both the prevalence of group I beta-lactamase-related resistance and the clinical setting in which resistance to expanded-spectrum cephalosporins occurs. METHODS: Isolates of Enterobacter spp. were sensitivity tested to a range of antibiotics, and selected isolates were DNA fingerprinted by pulsed-field gel electrophoresis. The medical records of all patients with positive cultures for Enterobacter spp. were reviewed to determine the effect of previous antibiotic treatment on the susceptibility profile of these organisms. RESULTS: The crude incidence of colonization/infection (n = 315) was 0.51 per 100 patients and 0.73 per 1000 days of hospitalization. The 4-day and 7-day Kaplan-Meier rates of colonization/infection with Enterobacter were estimated to be 7.57% (standard deviation (SD = 3.26%) and 4.16% (SD = 2.88%)), respectively. The time lag to colonization/infection with isolates producing large amounts of Bush group 1 beta-lactamase (HLBL) (27.35 +/- 27.30 days) was significantly different from that to colonization/infection with wild-type isolates (13.59 +/- 17.93 days) (P = 0.036). Ninety-six isolates (30.5%) demonstrated acquired resistance to expanded-spectrum cephalosporins: 34 isolates (10.8%) produced extended-spectrum beta-lactamase, and 62 isolates (19.7%) produced HLBL. The 89 Enterobacter isolates susceptible to third-generation cephalosporins yielded 84 major DNA patterns, and the 45 HLBL isolates yielded 38 major DNA patterns. The risk of colonization/infection with HLBL-producing Enterobacter was higher in cases of antimicrobial treatment with third-generation cephalosporins or a fluoroquinolone, and in cases of urinary tract colonization/infection. CONCLUSIONS: The judicious use in hospitals of both expanded-spectrum cephalosporins and other antibiotics such as fluoroquinolones is necessary to curtail the emergence of resistance in Enterobacter spp.

Cephalosporins↗

Clinical and molecular epidemiology of hospital Enterococcus faecium isolates in eastern France. Members of Réseau Franc-Comtois de Lutte contr les Infections Nosocomiales.

We carried out a surveillance study of Enterococcus faecium isolates in the Franche-Comtéregion of France over three years. Clinical and epidemiological strains were characterized by antibiotype and genotype (pulsed field gel electrophoresis, PFGE). Three case-control studies were performed to identify risk factors for colonization/infection with three defined resistant phenotypes (amoxycillin, high-level gentamicin and high-level kanamycin). The crude incidence of colonization/infection was 0.156%, and 68.8% of cases were classified as hospital-acquired. Incidence did not differ according to the type of hospitalization (middle term or acute care). The urinary tract was the major site of infection. Resistance rates were: 45.8% (amoxycillin), 18.7% (high-level gentamicin), 61.4% (high-level kanamycin) and 3.1% (vancomycin). No isolate produced b-lactamase and one isolate carried the vanA gene. PFGE revealed two major epidemic patterns each including resistant strains isolated in different hospitals and during different periods in the study. Previous antimicrobial treatment was not identified as a risk factor for colonization/infection with any resistant phenotype. Despite the low frequency of vancomycin-resistant isolates in this study, resistant strains were widely disseminated and had characteristics enabling them to persist and spread. If these strains acquired the vanA gene, the risk of an outbreak would be large. So, the prevalence of vancomycin-resistant E. faecium in hospitals should be carefully monitored in the future.

Adult↗

Molecular and functional characterization of an amphibian urea transporter.

We report the characterization of a frog (Rana esculenta) urea transporter (fUT). The cloned cDNA is 1.4 kb long and contains a putative open reading frame of 1203 bp. In frog urinary bladder, the gene is expressed as two mRNAs of 4.3 and 1.6 kb. The fUT protein is 63.1 and 56.3% identical to rat UT-A2 and UT-B1, respectively. The internal duplication of UT-A2 and UT-B, as well as the double LP box urea transporter signature sequence were found in this amphibian urea transporter. When expressed in Xenopus oocytes, fUT induced a 10-fold increase in urea permeability, which was blocked by both phloretin and mercurial reagents. The fUT protein did not transport thiourea, but the fUT-mediated urea transport was strongly inhibited by this compound. Thus, this amphibian urea transporter displays transport characteristics in between those of UT-A2 and UT-B.

Amino Acid Sequence↗

At physiological expression levels the Kidd blood group/urea transporter protein is not a water channel.

The Kidd (JK) blood group locus encodes a urea transporter that is expressed on human red cells and on endothelial cells of the vasa recta in the kidney. Here, we report the identification in human erythroblasts of a novel cDNA, designated HUT11A, which encodes a protein identical to the previously reported erythroid HUT11 urea transporter, except for a Lys(44) --> Glu substitution and a Val-Gly dipeptide deletion after proline 227, which leads to a polypeptide of 389 residues versus 391 in HUT11. Genomic typing by polymerase chain reaction and transcript analysis by ribonuclease protection assay demonstrated that HUT11A encodes the true Kidd blood group/urea transporter protein, which carries only 2 Val-Gly motifs. Upon expression at high levels in Xenopus oocytes, the physiological Kidd/urea transporter HUT11A conferred a rapid transfer of urea (which was insensitive to p-chloromercuribenzene sulfonate or phloretin), a high water permeability, and a selective uptake of small solutes including amides and diols, but not glycerol and meso-erythritol. However, at plasma membrane expression levels close to the level observed in the red cell membrane, HUT11A-mediated water transport and small solutes uptake were absent and the urea transport was poorly inhibited by p-chloromercuribenzene sulfonate, but strongly inhibited by phloretin. These findings show that, at physiological expression levels, the HUT11A transporter confers urea permeability but not water permeability, and that the observed water permeability is a feature of the red cell urea transporter when expressed at unphysiological high levels.

Amino Acid Sequence↗