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Войти в исследования European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2024
Ciprofloxacin-susceptible but levofloxacin-resistant Pseudomonas aeruginosa clinical strains with Vitek®2: which mechanism involved and consequences in case of fluoroquinolone treatment?
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Robert Manon, Ruffier d'Epenoux Louise, Paquin Axelle, Boutoille David, Guillouzouic Aurélie, Corvec Stéphane
Аннотация
PURPOSE: Pseudomonas aeruginosa clinical strains isolated harbored sometimes an atypical phenotype using the automated Vitek2®: ciprofloxacin-susceptibility but levofloxacin-resistance according to 2019 CA-SFM criteria. The aims of this study are to investigate the resistance mechanism(s) involved and to identify the consequences on fluoroquinolone treatment.
METHODS: Strain resistance profile, patient's data were recovered and reviewed from the database. Minimum inhibitory concentrations of levofloxacin, ciprofloxacin, moxifloxacin and delafloxacin were determined by using a concentration gradient strip. gyrA, gyrB, parC, parE and mexR genes were PCR amplified and sequenced. A PFGE analysis was performed for strains, recovered in a short period of time from the same patient.
RESULTS: 46 strains were studied. A couple of seldom mutations were detected in gyrA, gyrB, parC and parE genes. Phenotypically, most of the strains (91%) were resistant to ticarcillin/ clavulanic acid combination and aztreonam suggesting a MexAB-OprM efflux-pump overexpression. mexR sequencing demonstrated either a deletion, a mutation or a premature stop codon appearance leading to amino acid substitution for 75% of the strains. Interestingly, four patients presented successively a fully fluoroquinolone susceptible isolate, thereafter a ciprofloxacin-susceptible but levofloxacin-resistant isolate (discordant phenotype) and finally a fluoroquinolone-resistant isolate. Molecular typing of these strains highlighted a strong relatedness between those isolates.
CONCLUSION: The phenotype detected by the automate Vitek2® is linked to a likely efflux-pump overexpression mechanism and not fluoroquinolone-target mutation. Regarding this discordant phenotype, an alert should be provided to clinicians concerning the high risk of selecting a fluoroquinolone-resistant mutant.
METHODS: Strain resistance profile, patient's data were recovered and reviewed from the database. Minimum inhibitory concentrations of levofloxacin, ciprofloxacin, moxifloxacin and delafloxacin were determined by using a concentration gradient strip. gyrA, gyrB, parC, parE and mexR genes were PCR amplified and sequenced. A PFGE analysis was performed for strains, recovered in a short period of time from the same patient.
RESULTS: 46 strains were studied. A couple of seldom mutations were detected in gyrA, gyrB, parC and parE genes. Phenotypically, most of the strains (91%) were resistant to ticarcillin/ clavulanic acid combination and aztreonam suggesting a MexAB-OprM efflux-pump overexpression. mexR sequencing demonstrated either a deletion, a mutation or a premature stop codon appearance leading to amino acid substitution for 75% of the strains. Interestingly, four patients presented successively a fully fluoroquinolone susceptible isolate, thereafter a ciprofloxacin-susceptible but levofloxacin-resistant isolate (discordant phenotype) and finally a fluoroquinolone-resistant isolate. Molecular typing of these strains highlighted a strong relatedness between those isolates.
CONCLUSION: The phenotype detected by the automate Vitek2® is linked to a likely efflux-pump overexpression mechanism and not fluoroquinolone-target mutation. Regarding this discordant phenotype, an alert should be provided to clinicians concerning the high risk of selecting a fluoroquinolone-resistant mutant.