2020Open Forum Infectious DiseasesOpen access

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

Alexander Lawandi, Samuel De l’Étoile-Morel, Gleice Cristina Leite, Todd C. Lee

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Abstract

Abstract 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. Disclosures All Authors: No reported disclosures

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Abstract 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. Disclosures All Authors: No reported disclosures

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Abstract 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. Disclosures All Authors: No reported disclosures

Key concepts: Piperacillin, Tazobactam, Piperacillin/tazobactam, Klebsiella pneumoniae, Ceftriaxone, Microbiology, Beta-Lactamase Inhibitors, Medicine

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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 — Research Paper | ScholarLens