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dc.contributor.author | Butler, David A. | |
dc.contributor.author | Rana, Amisha P. | |
dc.contributor.author | Krapp, Fiorella | |
dc.contributor.author | Patel, Shitalben R. | |
dc.contributor.author | Huang, Yanqin | |
dc.contributor.author | Ozer, Egon A. | |
dc.contributor.author | Hauser, Alan R. | |
dc.contributor.author | Bulman, Zackery P. | |
dc.date.accessioned | 2021-04-13T20:51:01Z | |
dc.date.available | 2021-04-13T20:51:01Z | |
dc.date.issued | 2021 | |
dc.identifier.uri | https://hdl.handle.net/20.500.12866/9174 | |
dc.description.abstract | OBJECTIVES: KPC-producing Klebsiella pneumoniae (KPC-Kp) isolates commonly co-harbour the aminoglycoside-modifying enzyme (AME) gene aac(6')-Ib, which encodes an AME that can confer resistance to some of the commercially available aminoglycosides. We sought to determine the influence of AAC(6')-Ib in KPC-Kp on the pharmacodynamic activity of aminoglycosides. METHODS: Six KPC-Kp clinical isolates, three with and three without aac(6')-Ib, were analysed. Using these isolates, the bacterial killing of amikacin, gentamicin and tobramycin was assessed in static time-kill experiments. The pharmacodynamic activity of the aminoglycosides was then assessed in a dynamic one-compartment infection model over 72 h using simulated human pharmacokinetics of once-daily dosing with amikacin (15 mg/kg), gentamicin (5 mg/kg) and tobramycin (5 mg/kg). RESULTS: At clinically relevant aminoglycoside concentrations in time-kill experiments and the dynamic one-compartment model, gentamicin was more active than amikacin or tobramycin against the isolates harbouring aac(6')-Ib. Amikacin, gentamicin and tobramycin all showed progressively reduced bacterial killing with exposure to repeated doses against most isolates in the dynamic one-compartment model. MIC values were generally not a good predictor of gentamicin pharmacodynamic activity against KPC-Kp, but were more reliable for amikacin and tobramycin. CONCLUSIONS: Gentamicin may be preferred over amikacin or tobramycin for treatment of KPC-Kp infections. However, gentamicin MICs are not a consistent predictor of its pharmacodynamic activity and unexpected treatment failures are possible. | en_US |
dc.language.iso | eng | |
dc.publisher | Oxford University Press | |
dc.relation.ispartofseries | Journal of Antimicrobial Chemotherapy | |
dc.rights | info:eu-repo/semantics/restrictedAccess | |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/4.0/deed.es | |
dc.subject | Gentamicin sulfate (usp) | en_US |
dc.subject | amikacin | en_US |
dc.subject | genes | en_US |
dc.subject | gentamicins | en_US |
dc.subject | klebsiella | en_US |
dc.subject | pneumoniae | en_US |
dc.subject | infections | en_US |
dc.subject | enzymes | en_US |
dc.subject | tobramycin | en_US |
dc.subject | pharmacodynamics | en_US |
dc.subject | aminoglycosides | en_US |
dc.subject | killing | en_US |
dc.subject | malnutrition-inflammation-cachexia syndrome | en_US |
dc.subject | augmentative and alternative communication. | en_US |
dc.title | Optimizing aminoglycoside selection for KPC-producing Klebsiella pneumoniae with the aminoglycoside-modifying enzyme (AME) gene aac(6')-Ib | en_US |
dc.type | info:eu-repo/semantics/article | |
dc.identifier.doi | https://doi.org/10.1093/jac/dkaa480 | |
dc.subject.ocde | https://purl.org/pe-repo/ocde/ford#3.03.08 | |
dc.subject.ocde | https://purl.org/pe-repo/ocde/ford#3.01.05 | |
dc.subject.ocde | https://purl.org/pe-repo/ocde/ford#1.06.01 | |
dc.relation.issn | 1460-2091 |
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