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Journal of Clinical Microbiology, September 2003, p. 4246-4251, Vol. 41, No. 9
0095-1137/03/$08.00+0     DOI: 10.1128/JCM.41.9.4246-4251.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Presence of Pseudomonas putida Strains Harboring Plasmids Bearing the Metallo-ß-Lactamase Gene blaIMP in a Hospital in Japan

Sachie Yomoda,1 Toyoji Okubo,2 Ayako Takahashi,1 Masami Murakami,1 and Shizuko Iyobe2*

Department of Laboratory Medicine and Clinical Laboratory Center,1 Laboratory of Drug Resistance in Bacteria, Gunma University School of Medicine, 3-39-22, Showa-machi, Maebashi 371-8511, Japan2

Received 13 March 2003/ Returned for modification 18 April 2003/ Accepted 30 June 2003

To determine the persistence and spread of antibiotic-resistant strains in Gunma University Hospital, 83 Pseudomonas putida strains (each from a different patient) were isolated from January 1997 through December 2001. Of the 83 strains isolated, 27 were resistant to carbapenems. All 27 produced metallo-ß-lactamase and were found to be PCR positive for the blaIMP gene. Most (22 strains) were primarily isolated from the wards (W7 [9 strains] and W4 [8 strains]). Another five blaIMP-positive P. putida strains from wards W7 and W4 were obtained by swabbing around the water pipes. A total of 32 blaIMP-positive P. putida strains were assessed by pulsed-field gel electrophoresis (PFGE) and testing of drug susceptibility to 10 chemotherapeutic agents. Both PFGE and MIC patterns revealed that there were long-term resident strains among inpatients and hospital environments. The blaIMP genes of 22 of 32 strains were all transferable to a recipient strain of Pseudomonas aeruginosa by conjugation or transformation and conferred resistance to carbapenems and cephems. The blaIMP plasmids were conjugally transmissible among P. aeruginosa strains and mediated resistance to amikacin as well as ß-lactams. Ten of the 22 plasmids mediated additional resistance to gentamicin and tobramycin. Plasmids with identical DNA and drug resistance patterns were found in P. putida strains with identical PFGE patterns and with different PFGE patterns. We presumed that P. putida was one of the resident species in inpatients and especially in hospital environments, spreading drug resistance genes via plasmids among P. putida strains and supplying them to more pathogenically important species, such as P. aeruginosa.


* Corresponding author. Mailing address: Laboratory of Drug Resistance in Bacteria, Gunma University School of Medicine, 3-39-22, Showa-machi, Maebashi 371-8511, Japan. Phone: 81-27-220-8085. Fax: 81-27-220-8088. E-mail: siyobe{at}med.gunma-u.ac.jp.


Journal of Clinical Microbiology, September 2003, p. 4246-4251, Vol. 41, No. 9
0095-1137/03/$08.00+0     DOI: 10.1128/JCM.41.9.4246-4251.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:

  • Horii, T., Muramatsu, H., Iinuma, Y. (2005). Mechanisms of resistance to fluoroquinolones and carbapenems in Pseudomonas putida. J Antimicrob Chemother 56: 643-647 [Abstract] [Full Text]  
  • Walsh, T. R., Toleman, M. A., Poirel, L., Nordmann, P. (2005). Metallo-{beta}-Lactamases: the Quiet before the Storm?. Clin. Microbiol. Rev. 18: 306-325 [Abstract] [Full Text]