Abstract
Antibiotic resistance is a global health priority. Major defenses for Gram-negative bacteria are β-lactamase enzymes, which have co-evolved with the development and increasing utilization of new antibiotics. Bacteria harboring the plasmid-mediated AmpC enzymes are increasingly prevalent among adult patients, but have not previously been reported in neonates. Early-onset neonatal meningitis caused by an AmpC β-lactamase-producing Escherichia coli is described for the first time; the plasmid was identified as a transferable CMY-2 family β-lactamase. Limited experience with newer antibiotics and pharmacokinetics in neonates presents a therapeutic challenge. Currently, there are no Clinical Laboratory Standards Institute (CLSI) recommendations for detecting AmpC nor is the optimal treatment for AmpC-producing organisms known. Thus, it is imperative that clinicians have a high index of suspicion when antimicrobial susceptibility patterns are inconsistent. Development of better microbiology screening tests to rapidly detect resistance is essential. Additionally, pharmacokinetic studies with newer antibiotics in neonates are warranted.
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Acknowledgements
We gratefully acknowledge Wenchi Shan for designing the primers for the CMY plasmid and Andrew Campbell for critical reading of the manuscript.
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Fakioglu, E., Queenan, A., Bush, K. et al. Amp C β-lactamase-producing Escherichia coli in neonatal meningitis: diagnostic and therapeutic challenge. J Perinatol 26, 515–517 (2006). https://doi.org/10.1038/sj.jp.7211550
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DOI: https://doi.org/10.1038/sj.jp.7211550
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