Paradoxical effect ofKlebsiella pneumoniaeOmpK36 porin deficiency

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To evaluate the effect of defined mutations in the major OmpK35 and OmpK36 porins in Klebsiella pneumoniae on the activity of two common plasmid-mediated AmpC enzymes.


Naturally occurring conjugative plasmids containing blaDHA-1 and blaCMY-2 were obtained from K. pneumoniae isolates in western Sydney. These were moved into K. pneumoniae ATCC13883 and isogenic porin knockouts Kp885 (ΔompK35) and Kp886 (ΔompK36), created by homologous recombination of kanamycin resistance cartridges into the specified genes, and their antimicrobial susceptibilities compared.


β-lactam resistance was greater in the presence of CMY-2-containing plasmids than DHA-1-containing plasmids, and higher in K. pneumoniae than Escherichia coli. Neither cefepime nor imipenem resistance was observed, and DHA-mediated cefotaxime and ticarcillin/clavulanate resistance was unexpectedly reduced from 8–24 (CTX) and >256 (TIM) mg/L in Kp13883 to 1–2 (CTX) and 32–48 mg/L (TIM) in the isogenic ΔompK36 porin knockout Kp886.


AmpC plasmids in particular are an important cause of transmissible resistance to ticarcillin/clavulanate in K. pneumoniae, but probably not in E. coli. Single knockouts of OmpK35 and OmpK36 porins in K. pneumoniae do not significantly increase antibiotic resistance in K. pneumoniae, and a paradoxical lowering of resistance to CTX and TIM is seen with deletion of ompK36. This has potentially important clinical implications.

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