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Title: Detection of KPC-2 in a Clinical Isolate of Proteus mirabilis and First Reported Description of Carbapenemase Resistance Caused by a KPC Beta-Lactamase in P. mirabilis

Author
item TIBBETTS, ROBERT - WASHINGTON UNIVERSITY
item Frye, Jonathan
item DUNNE, WILLIAM - WASHINGTON UNIVERSITY

Submitted to: Journal of Clinical Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/16/2008
Publication Date: 9/1/2008
Citation: Tibbetts, R., Frye, J.G., Dunne, W. Detection of KPC-2 in a Clinical Isolate of Proteus mirabilis and First Reported Description of Carbapenemase Resistance Caused by a KPC Beta-Lactamase in P. mirabilis. Journal of Clinical Microbiology. 46(9):3080-3083.

Interpretive Summary: Resistance to beta-lactam antibiotics is increasingly found in a number of US bacterial isolates associated with clinical disease. This resistance may result in difficult to treat infections and/or increases in morbidity or mortality. Therefore a study was initiated to screen bacterial clinical isolates for resistance and to determine the mechanisms causing resistance. An isolate of Proteus mirabilis recovered from clinical cultures was shown to be resistant to the beta-lactams imipenem, meropenem, and ertapenem by disk diffusion susceptibility testing. PCR amplification of whole cell and/or plasmid DNA recovered from the isolate and sequence analysis determined that it harbored the blaKPC-2 gene on a transferable plasmid. This is a first report of carbapenem resistance in Proteus mirabilis caused by the acquisition of blaKPC. These results indicate that resistance to carbepenems has spread among the Enterobacteriacia. Additionally, clinical isolates of these Gram negative bacteria should be screened for resistance in order to optimize therapy.

Technical Abstract: An isolate of Proteus mirabilis recovered from bacterial cultures was shown to be resistant to imipenem, meropenem, and ertapenem by disk diffusion susceptibility testing. Amplification of whole cell and/or plasmid DNA recovered from the isolate using primers specific for the blaKPC carbapenemase gene produced an amplicon of the expected size which was confirmed to be blaKPC-2 by sequence analysis. Transformation of a susceptible E. coli host using plasmid preparations from the isolate generated a transformant with a 3-4 fold increase in the MIC to all carbapenems tested. We believe this to be the first report of carbapenem resistance in Proteus mirabilis caused by the acquisition of blaKPC.