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Antimicrobial Agents and Chemotherapy, April 2004, p. 1295-1299, Vol. 48, No. 4
0066-4804/04/$08.00+0     DOI: 10.1128/AAC.48.4.1295-1299.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Emerging Plasmid-Mediated Quinolone Resistance Associated with the qnr Gene in Klebsiella pneumoniae Clinical Isolates in the United States

Minggui Wang,1,2 Daniel F. Sahm,3 George A. Jacoby,4 and David C. Hooper1*

Division of Infectious Diseases, Massachusetts General Hospital, Boston, Massachusetts 02114,1 Institute of Antibiotics, Huashan Hospital, Fudan University, Shanghai 200040, China,2 Focus Technologies, Herndon, Virginia 20171,3 Infectious Disease Department, Lahey Clinic, Burlington, Massachusetts 018054

Received 10 October 2003/ Returned for modification 19 December 2003/ Accepted 30 December 2003

Although quinolone resistance commonly results from chromosomal mutation, recent studies indicate that such resistance can also be transferred on plasmids carrying the gene responsible, qnr. One hundred ten ciprofloxacin-resistant clinical isolates of Klebsiella pneumoniae and Escherichia coli from the United States were screened for the qnr gene by PCR and Southern hybridization of plasmid DNA. Conjugation experiments were done with azide-resistant E. coli J53 as the recipient and selection with azide and sulfonamide, a resistance frequently linked to qnr. EcoRI and BamHI digests of qnr-hybridizing plasmids were subjected to electrophoresis on agarose gels and probed with qnr by Southern hybridization. qnr was detected in 8 (11.1%) of 72 K. pneumoniae strains. These eight positive strains were from six states in the United States. qnr was not found in any of the 38 E. coli strains tested. Quinolone resistance was transferred from seven of the eight probe-positive strains. Transconjugants with qnr-hybridizing plasmids had 32-fold increases in ciprofloxacin MICs relative to E. coli J53. For all eight strains, the sequence of qnr was identical to that originally reported. By size and restriction digests, four plasmids were related to the first-reported plasmid, pMG252, and three were different. Five new qnr plasmids encoded FOX-5 ß-lactamase, as did pMG252, but two others produced SHV-7 extended-spectrum ß-lactamase. Transferable plasmid-mediated quinolone resistance associated with qnr is now widely distributed in quinolone-resistant clinical strains of K. pneumoniae in the United States. Plasmid-determined quinolone resistance contributes to the increasing quinolone resistance of K. pneumoniae isolates and to the linkage previously observed between resistance to quinolones and the latest ß-lactam antibiotics.

* Corresponding author. Mailing address: Division of Infectious Diseases, Massachusetts General Hospital, 55 Fruit St., Boston, MA 02114-2696. Phone: (617) 726-3812. Fax: (617) 726-7416. E-mail: dhooper{at}partners.org.

Antimicrobial Agents and Chemotherapy, April 2004, p. 1295-1299, Vol. 48, No. 4
0066-4804/04/$08.00+0     DOI: 10.1128/AAC.48.4.1295-1299.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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