Steininger 2002 J Antimicrob Chemother: Difference between revisions
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{{Publication | {{Publication | ||
|title=Steininger C, Allerberger F, Gnaiger E (2002) Clinical significance of inhibition kinetics in Streptococcus pyogenes in response to penicillin. J Antimicrob Chemother 50: 517- | |title=Steininger C, Allerberger F, Gnaiger E (2002) Clinical significance of inhibition kinetics in ''Streptococcus pyogenes'' in response to penicillin. J Antimicrob Chemother 50:517-23. https://doi.org/10.1093/jac/dkf174 | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/12356796 PMID: 12356796] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/12356796 PMID: 12356796 Open Access] | ||
|authors=Steininger C, Allerberger F, Gnaiger | |authors=Steininger C, Allerberger F, Gnaiger Erich | ||
|year=2002 | |year=2002 | ||
|journal=J Antimicrob Chemother | |journal=J Antimicrob Chemother | ||
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Results: None of the clinical isolates exhibited penicillin tolerance. Latency in the respirometric response of ''S. pyogenes'' to penicillin increased significantly with decreasing strain-specific respirometric growth rate. No difference in inhibition kinetics was found in vitro for isolates from patients with or without bacteriological treatment failure. | Results: None of the clinical isolates exhibited penicillin tolerance. Latency in the respirometric response of ''S. pyogenes'' to penicillin increased significantly with decreasing strain-specific respirometric growth rate. No difference in inhibition kinetics was found in vitro for isolates from patients with or without bacteriological treatment failure. | ||
Conclusions: In streptococcal pharyngotonsillitis, tolerance is not a relevant concept to explain bacteriological treatment failure. Definitions of tolerance should be reconsidered in the framework of growth-dependent antibiotic susceptibility. | Conclusions: In streptococcal pharyngotonsillitis, tolerance is not a relevant concept to explain bacteriological treatment failure. Definitions of tolerance should be reconsidered in the framework of growth-dependent antibiotic susceptibility. | ||
|mipnetlab= | |mipnetlab=AT Innsbruck Gnaiger E, AT Innsbruck Oroboros | ||
}} | }} | ||
== Cited by == | |||
::* 2 articles in PubMed (2021-12-27) https://pubmed.ncbi.nlm.nih.gov/12356796/ | |||
{{Labeling | {{Labeling | ||
|area=Respiration, mt-Biogenesis;mt-density, mt-Medicine, Pharmacology;toxicology | |||
|diseases=Infectious | |||
|organism=Eubacteria | |||
|preparations=Intact cells | |||
|couplingstates=ROUTINE | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
}} | }} |
Latest revision as of 09:45, 27 March 2024
Steininger C, Allerberger F, Gnaiger E (2002) Clinical significance of inhibition kinetics in Streptococcus pyogenes in response to penicillin. J Antimicrob Chemother 50:517-23. https://doi.org/10.1093/jac/dkf174 |
Steininger C, Allerberger F, Gnaiger Erich (2002) J Antimicrob Chemother
Abstract: Objectives: The antibiotic mode of action against clinical isolates of Streptococcus pyogenes and physiological factors involved in modifying the inhibitory response to the antibiotic were investigated. Methods: We developed high-resolution respirometry for continuous monitoring of bacterial growth and inhibition kinetics. One hundred and ten clinical isolates from 90 paediatric patients were tested, including 48 isolates obtained from 28 patients with eradication failure. Respirometric inhibition curves were monitored at 4 mg/L penicillin G over a short 30 min period, corresponding to the drugโs serum half-life.
Results: None of the clinical isolates exhibited penicillin tolerance. Latency in the respirometric response of S. pyogenes to penicillin increased significantly with decreasing strain-specific respirometric growth rate. No difference in inhibition kinetics was found in vitro for isolates from patients with or without bacteriological treatment failure. Conclusions: In streptococcal pharyngotonsillitis, tolerance is not a relevant concept to explain bacteriological treatment failure. Definitions of tolerance should be reconsidered in the framework of growth-dependent antibiotic susceptibility.
โข O2k-Network Lab: AT Innsbruck Gnaiger E, AT Innsbruck Oroboros
Cited by
- 2 articles in PubMed (2021-12-27) https://pubmed.ncbi.nlm.nih.gov/12356796/
Labels: MiParea: Respiration, mt-Biogenesis;mt-density, mt-Medicine, Pharmacology;toxicology
Pathology: Infectious
Organism: Eubacteria
Preparation: Intact cells
Coupling state: ROUTINE
HRR: Oxygraph-2k