ArticleThe Journal of infectious diseases2024
What Contributes to the Minimum Inhibitory Concentration? Beyond β-Lactamase Gene Detection in Klebsiella pneumoniae.
Article in The Journal of infectious diseases, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- IncL plasmid-mediated dissemination of OXA-48 β-lactamase andJAC-antimicrobial resistance · 2026Article
- Recurrent Polymicrobial Bloodstream Infection in End-Stage Renal Disease: Co-Infection withInternational medical case reports journal · 2026Article
- Comprehensive Assessment of Initial Adaptation of Extended-Spectrum β-Lactamase-Positive ST131 Escherichia coli to Carbapenem Exposure.The Journal of infectious diseases · 2025Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundKlebsiella pneumoniae is capable of resistance to β-lactam antibiotics through expression of β-lactamases (both chromosomal and plasmid-encoded) and downregulation of outer membrane porins. However, the extent to which these mechanisms interplay in a resistant phenotype is not well understood. The purpose of this study was to determine the extent to which β-lactamases and outer membrane porins affected β-lactam resistance.
methodsMinimum inhibitory concentrations (MICs) to β-lactams and inhibitor combinations were determined by agar dilution or Etest. Outer membrane porin production was evaluated by Western blot of outer membrane fractions. β-lactamase carriage was determined by whole genome sequencing and expression evaluated by real-time reverse-transcription polymerase chain reaction.
resultsPlasmid-encoded β--lactamases were important for cefotaxime and ceftazidime resistance. Elevated expression of chromosomal SHV was important for ceftolozane-tazobactam resistance. Loss of outer membrane porins was predictive of meropenem resistance. Extended-spectrum β-lactamases and plasmid-encoded AmpCs (pAmpCs) in addition to porin loss were sufficient to confer resistance to the third-generation cephalosporins, piperacillin-tazobactam, ceftolozane-tazobactam, and meropenem. pAmpCs (CMY-2 and DHA) alone conferred resistance to piperacillin-tazobactam.
conclusionsDetection of a resistance gene by whole genome sequencing was not sufficient to predict resistance to all antibiotics tested. Some β-lactam resistance was dependent on the expression of both plasmid-encoded and chromosomal β-lactamases and loss of porins.
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