646 - Adapting the modified Carbapenem Inactivation Method to assess for possible beta-lactamase mediated resistance in Piperacillin-Tazobactam resistant/ Ceftriaxone susceptible Escherichia. coli and Klebsiella pneumoniae

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Presenting Author(s)

Alexander Lawandi

Fellow
Department of Critical Care Medicine, National Institutes of Health Clinical Center
Bethesda, Maryland
Disclosure: I do not have any relevant financial / non-financial relationships with any proprietary interests.

Co-Author(s)

SD

Samuel De L'Etoile-Morel

Fellow
McGill University Health Centre
Montreal, Quebec, Canada
Disclosure: I do not have any relevant financial / non-financial relationships with any proprietary interests.
GL

Gleice C. Leite

Research Associate
McGill University Health Centre
Montreal, Quebec, Canada
Disclosure: I do not have any relevant financial / non-financial relationships with any proprietary interests.
TL

Todd C. Lee

Associate Professor of Medicine
McGill University
Montreal, Quebec, Canada
Disclosure: I do not have any relevant financial / non-financial relationships with any proprietary interests.

Background: A cluster of piperacillin-tazobactam resistant/ceftriaxone susceptible Escherichia coli and Klebsiella pneumonaie bacteremias were noted at our institution. A review of the literature suggested this resistance phenotype was mediated by a beta-lactamase. We sought to further corroborate this phenotypically.

Methods: We adapted the "carbapenem inactivation method" utilizing piperacillin-tazobactam and ceftriaxone discs on all E. coli and K. pneumoniae isolated from blood and demonstrating piperacillin-tazobactam resistance but with ceftriaxone susceptibility. We utilized pan-susceptible and carbapenem resistance Enterobacteriaceae reference strains as well as third generation cephalosporin resistant, piperacillin-tazobactam susceptible isolates as controls.

Results: 96% of the piperacillin-tazobactam resistant, ceftriaxone susceptible strains demonstrated the capacity to degrade the piperacillin-tazobactam discs while 100% spared the ceftriaxone discs. 75% of the piperacillin-tazobactam susceptible, ceftriaxone resistant control strains spared the piperacillin-tazobactam discs while degrading the ceftriaxone discs.

Conclusion: The resistance phenotype observed is due to beta-lactamase production and the modified carbapenem inactivation method can be adapted to probe for other beta-lactamases. Further study is required to definitively identify which beta-lactamase is responsible.