Paradoxical effect of Klebsiella pneumoniae OmpK36 porin deficiency

Xiuhong Jiang; Bjorn Espedido; Sally R. Partridge; Lee C. Thomas; Feng Wang; Jonathan R. Iredell

Paradoxical effect of Klebsiella pneumoniae OmpK36 porin deficiency

Xiuhong Jiang
, Bjorn Espedido
, Sally R. Partridge
, Lee C. Thomas
, Feng Wang
, Jonathan R. Iredell

Research output: Contribution to journal › Article

9 Citations (Scopus)

Abstract

The aim of this study was 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 (DompK35) and Kp886 (DompK36), created by homologous recombination of kanamycin resistance cartridges into the specified genes, and their antimicrobial susceptibilities compared. b-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 DHAmediated cefotaxime and ticarcillin/clavulanate resistance was unexpectedly reduced from 8ÃƒÂ¢Ã¢"šÂ¬Ã¢â‚¬Å“24 (CTX) and 4256 (TIM) mg/L in Kp13883 to 1ÃƒÂ¢Ã¢"šÂ¬Ã¢â‚¬Å“2 (CTX) and 32ÃƒÂ¢Ã¢"šÂ¬Ã¢â‚¬Å“48 mg/L (TIM) in the isogenic DompK36 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.

Original language	English
Pages (from-to)	388-392
Number of pages	5
Journal	Pathology
Volume	41
Issue number	4
Publication status	Published - 2009

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

Klebsiella pneumoniae
drug resistance in microorganisms

Cite this

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title = "Paradoxical effect of Klebsiella pneumoniae OmpK36 porin deficiency",

abstract = "The aim of this study was 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 (DompK35) and Kp886 (DompK36), created by homologous recombination of kanamycin resistance cartridges into the specified genes, and their antimicrobial susceptibilities compared. b-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 DHAmediated cefotaxime and ticarcillin/clavulanate resistance was unexpectedly reduced from 8{\~A}ƒ{\^A}¢{\~A}¢{"}{\v s}{\^A}¬{\~A}¢{\^a}‚¬{\AA}{\textquotedblleft}24 (CTX) and 4256 (TIM) mg/L in Kp13883 to 1{\~A}ƒ{\^A}¢{\~A}¢{"}{\v s}{\^A}¬{\~A}¢{\^a}‚¬{\AA}{\textquotedblleft}2 (CTX) and 32{\~A}ƒ{\^A}¢{\~A}¢{"}{\v s}{\^A}¬{\~A}¢{\^a}‚¬{\AA}{\textquotedblleft}48 mg/L (TIM) in the isogenic DompK36 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.",

keywords = "Klebsiella pneumoniae, drug resistance in microorganisms",

author = "Xiuhong Jiang and Bjorn Espedido and Partridge, \{Sally R.\} and Thomas, \{Lee C.\} and Feng Wang and Iredell, \{Jonathan R.\}",

year = "2009",

language = "English",

volume = "41",

pages = "388--392",

journal = "Pathology",

issn = "0031-3025",

publisher = "Elsevier B.V.",

number = "4",

}

TY - JOUR

T1 - Paradoxical effect of Klebsiella pneumoniae OmpK36 porin deficiency

AU - Jiang, Xiuhong

AU - Espedido, Bjorn

AU - Partridge, Sally R.

AU - Thomas, Lee C.

AU - Wang, Feng

AU - Iredell, Jonathan R.

PY - 2009

Y1 - 2009

N2 - The aim of this study was 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 (DompK35) and Kp886 (DompK36), created by homologous recombination of kanamycin resistance cartridges into the specified genes, and their antimicrobial susceptibilities compared. b-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 DHAmediated cefotaxime and ticarcillin/clavulanate resistance was unexpectedly reduced from 8ÃƒÂ¢Ã¢"šÂ¬Ã¢â‚¬Å“24 (CTX) and 4256 (TIM) mg/L in Kp13883 to 1ÃƒÂ¢Ã¢"šÂ¬Ã¢â‚¬Å“2 (CTX) and 32ÃƒÂ¢Ã¢"šÂ¬Ã¢â‚¬Å“48 mg/L (TIM) in the isogenic DompK36 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.

AB - The aim of this study was 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 (DompK35) and Kp886 (DompK36), created by homologous recombination of kanamycin resistance cartridges into the specified genes, and their antimicrobial susceptibilities compared. b-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 DHAmediated cefotaxime and ticarcillin/clavulanate resistance was unexpectedly reduced from 8ÃƒÂ¢Ã¢"šÂ¬Ã¢â‚¬Å“24 (CTX) and 4256 (TIM) mg/L in Kp13883 to 1ÃƒÂ¢Ã¢"šÂ¬Ã¢â‚¬Å“2 (CTX) and 32ÃƒÂ¢Ã¢"šÂ¬Ã¢â‚¬Å“48 mg/L (TIM) in the isogenic DompK36 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.

KW - Klebsiella pneumoniae

KW - drug resistance in microorganisms

UR - http://handle.uws.edu.au:8081/1959.7/502621

M3 - Article

SN - 0031-3025

VL - 41

SP - 388

EP - 392

JO - Pathology

JF - Pathology

IS - 4

ER -

Paradoxical effect of Klebsiella pneumoniae OmpK36 porin deficiency

Abstract

UN SDGs

Keywords

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