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Determination of ciprofloxacin susceptibility in clinical isolates of Pseudomonas aeruginosa
A24 Clonal analysis of antibiotic resistant E.coli 0157 DH Mitwalli, FJR Abadi, F Thomson-Carter & TH Pennington, Department of Medical Microbiology, Aberdeen University, Aberdeen Al325 2ZD, UK Antimicrobial susceptibility testing was performed on 134 human and153 animal Scottish E.coZi 0157:H7 strains collected between 1992 and 1996. Eight anitimicrobial agents were tested based on their abundant clinical use in the treatment of urinary tract infections. All isolates were sensitive to gentamycin, cefotaxim, ciprofloxacin, and chloramphenicol. Sixteen human and 13 animal strains were resistant or intermediately resistant to one or more of the following: amoxycillin, amoxycillin and clavulinic acid, trimethoprim, and nitrofurantoin. Pulsed-field gel electrophoresis showed considerable diversity between the resistant strains revealing that these strains are not descendants from a single progenitor, and that various subtypes of E.coli 0157:H7 may develop antimicrobial resistance. Also, none of the resistant strains shared pulsed-field profiles with sensitive ones. Plasmid analysis of resistant strains demonstrated various profiles, however plasmids unique to resistant strains have not yet been identified. Emergence of resistance in E.coli 0157:H7 may complicate treatment, on the other hand, it may be used as a marker for tracing epidemiologically related strains in outbreak cases.
PSEUDOMONAS AERUGINOSA AND RESISTANCE TO CIPROFLOXACIN IN A SPINAL INJURIES UNIT - A LONGITUDINAL STUDY. J Wright, OM Murphy, G Dicldnson, A Galloway. Dept. Microbiology, Hexham General Hospital, Northumber1and, NE46 1QJ. Introduction: P. aeruginosa remains a cotnmon cause of infection in spinal injury patients. Antibiotic resistance, in
particular cipmfloxacin resistance,can result in therapeutic diflicultica. The aim of this studywas to study P. aeruginosa colonisationin a cohortof spinal injury patientsand monitor the development of cipmfloxacin resistance. Methods: Between October 1997 and July 1998 all isolates of P. aeruginosa, including sequential isolates, from patients attending the SJU were examined for ciprotloxacin resistance by E test and also semtyued. Results: 125 isolates of P. aeruginosa from 38 (1-16 isolates/patient)patients were examined. Twenty five patients (65.7%) bad 3 or more isolatea from various sites over a period of time. The majority (89%) of strains examined were isolated from urine. Ciprofloxacin resistance (.MlC >4mgL) was cktocted in 43%. Fourteen patients were colonised with resistant strains; 8 patients were colon&d with both a sensitive and a resistant strain. The majority (88%) were typeable by serotyping and 9 serotypes were found. Sixteen (42%) of patients had more than one serotypc isolated. No patient developed cipmfloxacii resistance but 2 patients did acquire resistant strains (different samtypes) during the study period. Conclusion: A sign&ant level of ciprofloxacin &stance was detected. Colonisation with multiple strains occurmd in a significant number of patients. Patients were more likely to acquire a cipmfloxacin resistant strain than to develop resistance in a de-novo strain.
FIS 98 Abstracts DETERMINATION OF CIPROFLOXACIN SUSCEPTIRILITY IN CLINICAL ISOLATES OF PSEUDOMONAS AERUGINOSA. J Wright, OM Murphy, G Dickinson, A Galloway. Department of Microbiology, Hexham General Hospital, Northumberland. NE46 1QJ. Background: Over-estimation of ciprofloxacin resistance in clinical isolates is well documented, This can result in therapeutic difficulties especially in the treatment of pseudomonas infection in spinal injury patients. We aimed to evaluate our current methodology in order to optimise management Methods:
of these patients.
104 isolates of P. aerugrnosa (previously reported as 50 ‘sensitive’ and 54 ‘resistant’) were re-evaluated using E teat, Stoke’s (3 and 7 mm cut of?) and a standard&d method. Results: E test MIC was considered the gold standard. Six isolates (5.8%) with MIC of l.SmgiI. had been reported as sensitive.Thirteen isolates(l2.5%) with MICs 1.0 - 3.01ug/L had been reported as resistant. Stoke’s method (BSAC interpretative criteria) correlated most accurately with E test but a significant number of categorisation errors still OcculTed. Conclusion: Correct datermination of P. aeruginosa ciprofloxacin susceptibility has therapeutic implications. Currently available methods are sub-optimal especially when the MIC ranges between 1.O - 4.Omg/L. Although, avoidance of major categorisation errors is important, in patients where oral anti-pseudomonal therapy offers both clinical and financial benefit, isolates with borderline susceptibility should be examined by E test.
INDUCED EXPRESSION OF A NOVEL Aspergillus fumigutus PUTATIVE DRUG EFFLUX GENE IN RESPONSE TO ITRACONAZOLE. J..&&y&, M.J. Anderson’, G.K. Dixon2, I.S. Roberts’ and D.W. Denning’, ‘Faculty of Medicine, University of Manchester, Manchester, UK and *Zeneca Pharmaceuticals, Macclesfield, UK. Two agents are licensed for the treatment of A. fumigates infection, amphotericin B and itraconazole. Resistance to itraconazole has been detected in vitro and has been validated in vivo. Studies of Saccharomyces cerevisiae and Can&da species have shown that one mechanism of azole resistance is drug efflux by ATP-binding cassette (ABC) transporters. An A.fitmigatus genomic library was screened with a probe f?om the C. albicans ABC transporter gene, CDRI. This screening revealed a novel gene, AfuMDR3, which had a high level of identity to other fungal multidrug resistance genes. Dot blot analysis showed that AfuMDR3 is upregulated by over 6-fold in a resistant isolate (AF72) which is unable to accumulate itraconazole. However, upregulation only occurred when AF72 was grown in sub-MIC concentrations of itraconazole. The regulation of this gene was also studied in response to heat shock, ethanol and other drugs, including fluconazole. AfuMDR3 is a novel ABC transporter, possibly involved in the efflux of itraconazole from A. fumigates. Complementation studies in yeast will be undertaken to establish the protein’s substrate range.
PSEUDOMONAS AERUGINOSA AND RESISTANCE TO CIPROFLOXACIN IN A SPINAL INJURIES UNIT - A LONGITUDINAL STUDY. J Wright, OM Murphy, G Dicldnson, A Galloway. Dept. Microbiology, Hexham General Hospital, Northumber1and, NE46 1QJ. Introduction: P. aeruginosa remains a cotnmon cause of infection in spinal injury patients. Antibiotic resistance, in
particular cipmfloxacin resistance,can result in therapeutic diflicultica. The aim of this studywas to study P. aeruginosa colonisationin a cohortof spinal injury patientsand monitor the development of cipmfloxacin resistance. Methods: Between October 1997 and July 1998 all isolates of P. aeruginosa, including sequential isolates, from patients attending the SJU were examined for ciprotloxacin resistance by E test and also semtyued. Results: 125 isolates of P. aeruginosa from 38 (1-16 isolates/patient)patients were examined. Twenty five patients (65.7%) bad 3 or more isolatea from various sites over a period of time. The majority (89%) of strains examined were isolated from urine. Ciprofloxacin resistance (.MlC >4mgL) was cktocted in 43%. Fourteen patients were colonised with resistant strains; 8 patients were colon&d with both a sensitive and a resistant strain. The majority (88%) were typeable by serotyping and 9 serotypes were found. Sixteen (42%) of patients had more than one serotypc isolated. No patient developed cipmfloxacii resistance but 2 patients did acquire resistant strains (different samtypes) during the study period. Conclusion: A sign&ant level of ciprofloxacin &stance was detected. Colonisation with multiple strains occurmd in a significant number of patients. Patients were more likely to acquire a cipmfloxacin resistant strain than to develop resistance in a de-novo strain.
FIS 98 Abstracts DETERMINATION OF CIPROFLOXACIN SUSCEPTIRILITY IN CLINICAL ISOLATES OF PSEUDOMONAS AERUGINOSA. J Wright, OM Murphy, G Dickinson, A Galloway. Department of Microbiology, Hexham General Hospital, Northumberland. NE46 1QJ. Background: Over-estimation of ciprofloxacin resistance in clinical isolates is well documented, This can result in therapeutic difficulties especially in the treatment of pseudomonas infection in spinal injury patients. We aimed to evaluate our current methodology in order to optimise management Methods:
of these patients.
104 isolates of P. aerugrnosa (previously reported as 50 ‘sensitive’ and 54 ‘resistant’) were re-evaluated using E teat, Stoke’s (3 and 7 mm cut of?) and a standard&d method. Results: E test MIC was considered the gold standard. Six isolates (5.8%) with MIC of l.SmgiI. had been reported as sensitive.Thirteen isolates(l2.5%) with MICs 1.0 - 3.01ug/L had been reported as resistant. Stoke’s method (BSAC interpretative criteria) correlated most accurately with E test but a significant number of categorisation errors still OcculTed. Conclusion: Correct datermination of P. aeruginosa ciprofloxacin susceptibility has therapeutic implications. Currently available methods are sub-optimal especially when the MIC ranges between 1.O - 4.Omg/L. Although, avoidance of major categorisation errors is important, in patients where oral anti-pseudomonal therapy offers both clinical and financial benefit, isolates with borderline susceptibility should be examined by E test.
INDUCED EXPRESSION OF A NOVEL Aspergillus fumigutus PUTATIVE DRUG EFFLUX GENE IN RESPONSE TO ITRACONAZOLE. J..&&y&, M.J. Anderson’, G.K. Dixon2, I.S. Roberts’ and D.W. Denning’, ‘Faculty of Medicine, University of Manchester, Manchester, UK and *Zeneca Pharmaceuticals, Macclesfield, UK. Two agents are licensed for the treatment of A. fumigates infection, amphotericin B and itraconazole. Resistance to itraconazole has been detected in vitro and has been validated in vivo. Studies of Saccharomyces cerevisiae and Can&da species have shown that one mechanism of azole resistance is drug efflux by ATP-binding cassette (ABC) transporters. An A.fitmigatus genomic library was screened with a probe f?om the C. albicans ABC transporter gene, CDRI. This screening revealed a novel gene, AfuMDR3, which had a high level of identity to other fungal multidrug resistance genes. Dot blot analysis showed that AfuMDR3 is upregulated by over 6-fold in a resistant isolate (AF72) which is unable to accumulate itraconazole. However, upregulation only occurred when AF72 was grown in sub-MIC concentrations of itraconazole. The regulation of this gene was also studied in response to heat shock, ethanol and other drugs, including fluconazole. AfuMDR3 is a novel ABC transporter, possibly involved in the efflux of itraconazole from A. fumigates. Complementation studies in yeast will be undertaken to establish the protein’s substrate range.