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Antimicrobial Agents and Chemotherapy, February 2007, p. 800-801, Vol. 51, No. 2
0066-4804/07/$08.00+0     doi:10.1128/AAC.01143-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

LETTER TO THE EDITOR

Klebsiella pneumoniae Isolate Producing at Least Eight Different ß-Lactamases, Including AmpC and KPC ß-Lactamases{triangledown}


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Reports of the production of multiple ß-lactamases in a single gram-negative pathogen are increasing (1, 2, 6). Isolates of Klebsiella species producing KPC-2, SHV extended-spectrum ß-lactamases (ESBLs), and inhibitor-resistant TEM-30 ß-lactamases have been reported as endemic in New York City (1). The present report identifies a Klebsiella pneumoniae isolate from New York City which produced up to 10 different ß-lactamases, including a FOX-like plasmid-mediated AmpC, in addition to the previously reported KPC, SHV ESBL, and IRT ß-lactamases (1).

The K. pneumoniae isolate was obtained from the sputum of a patient with a mesothelioma. No carbapenem antibiotics were given to the patient prior to the isolation of the K. pneumoniae isolate. CLSI (formerly NCCLS) disk diffusion and broth microdilution assays (4) revealed that the K. pneumoniae isolate lacked susceptibility to levofloxacin (>16 µg/ml), amikacin (32 µg/ml), piperacillin-tazobactam (>128 µg/ml), ceftazidime (128 µg/ml), cefotaxime (64 µg/ml), aztreonam (>128 µg/ml), and cefoxitin (>64 µg/ml) but was susceptible by microbroth tests to tigecycline (0.5 µg/ml), minocycline (4 µg/ml), polymyxin B (1 µg/ml), cefepime, and imipenem. However, when broth microdilution tests were performed with an inoculum of 107 CFU/ml instead of 105 CFU/ml, the MICs of both imipenem and cefepime increased (4 µg/ml to 32 µg/ml and 8 µg/ml to >128 µg/ml, respectively). The MICs of tigecycline, minocycline, and polymyxin B were not affected when a higher inoculum was used. The presence of an ESBL was indicated by the CLSI ESBL confirmatory disk tests but not by the CLSI ESBL broth microdilution confirmatory tests (4).

Isoelectric focusing (IEF) indicated that this isolate produced up to 10 different ß-lactamases. Characterization of these enzymes was performed, as previously described, using IEF, inhibitor profiles, cefotaxime gel hydrolysis assays, and PCR (5-7, 8, 9). Using these techniques, 8 of 10 ß-lactamases were identified. Three of these enzymes hydrolyzed cefotaxime. The pI and inhibitor profiles of these enzymes suggested the production of an SHV-12-like ESBL, a KPC-like carbapenem-hydrolyzing enzyme, a FOX-like AmpC, a PSE-1-like ß-lactamase, and an OXA ß-lactamase. In addition, TEM-1-like, TEM-30-like, and SHV-1-like enzymes were also identified (Table 1). PCR amplification using family-specific primers substantiated the presence of these genes within the K. pneumoniae isolate and identified the OXA ß-lactamase as an OXA-9-like ß-lactamase. Sequence data generated using the same primers that amplified the blaOXA product also suggested that the gene was blaOXA-9.


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  		TABLE 1. Identification of the ß-lactamases produced by the K. pneumoniae isolate

 
Accurate ß-lactam susceptibility testing can be expected to become increasingly difficult over the next few years due to an increase in isolates producing multiple ß-lactamases. The numbers and types of ß-lactamases produced by the K. pneumoniae isolate from New York described in this report are a cause for concern, especially with respect to detecting ESBL, AmpC, and KPC-type enzymes. The CLSI microbroth ESBL confirmatory tests were unable to detect the presence of the SHV ESBL in this isolate, and these tests also suggested imipenem susceptibility, even though the isolate produced a KPC-type enzyme. As the number of pathogens producing multiple ß-lactamases continues to rise, the difficulties in identifying the mechanisms responsible for ß-lactam MICs will increase (1, 2, 6, 10). Clinical laboratories need the option of molecular testing in addition to phenotypic testing for the identification of resistance mechanisms that may be masked by the production of multiple enzymes. Additional testing options for these highly resistant pathogens may help avert future outbreaks like the ones reported for KPC-producing K. pneumoniae isolates in New York (1-3).


   FOOTNOTES
 
{triangledown} Published ahead of print on 4 December 2006. Back


   REFERENCES
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  1. Bradford, P. A., S. Bratu, C. Urban, M. Visalli, N. Mariano, D. Landman, J. J. Rahal, S. Brooks, S. Cebular, and J. Quale. 2004. Emergence of carbapenem-resistant Klebsiella species possessing the class A carbapenem-hydrolyzing KPC-2 and inhibitor-resistant TEM-30 beta-lactamases in New York City. Clin. Infect. Dis. 39:55-60.[CrossRef][Medline]
  2. Bratu, S., D. Landman, R. Haag, R. Recco, A. Eramo, M. Alam, and J. Quale. 2005. Rapid spread of carbapenem-resistant Klebsiella pneumoniae in New York City: a new threat to our antibiotic armamentarium. Arch. Intern. Med. 165:1430-1435.[Abstract/Free Full Text]
  3. Bratu, S., M. Mooty, S. Nichani, D. Landman, C. Gullans, B. Pettinato, U. Karumudi, P. Tolaney, and J. Quale. 2005. Emergence of KPC-possessing Klebsiella pneumoniae in Brooklyn, New York: epidemiology and recommendations for detection. Antimicrob. Agents Chemother. 49:3018-3020.[Abstract/Free Full Text]
  4. Clinical and Laboratory Standards Institute. 2006. Performance standards for antimicrobial susceptibility testing. CLSI/NCCLS M100-S16. Clinical and Laboratory Standards Institute, Wayne, PA.
  5. Hanson, N. D., E. Smith Moland, and J. D. Pitout. 2001. Enzymatic characterization of TEM-63, a TEM-type extended spectrum beta-lactamase expressed in three different genera of Enterobacteriaceae from South Africa. Diagn. Microbiol. Infect. Dis. 40:199-201.[CrossRef][Medline]
  6. Hanson, N. D., K. S. Thomson, E. S. Moland, C. C. Sanders, G. Berthold, and R. G. Penn. 1999. Molecular characterization of a multiply resistant Klebsiella pneumoniae encoding ESBLs and a plasmid-mediated AmpC. J. Antimicrob. Chemother. 44:377-380.[Abstract/Free Full Text]
  7. Moland, E. S., N. D. Hanson, J. A. Black, A. Hossain, W. Song, and K. S. Thomson. 2006. Prevalence of newer beta-lactamases in gram-negative clinical isolates collected in the United States in 2001 to 2002. Antimicrob. Agents Chemother. 44:3318-3324.
  8. Perez-Perez, F. J., and N. D. Hanson. 2002. Detection of plasmid-mediated AmpC beta-lactamase genes in clinical isolates by using multiplex PCR. J. Clin. Microbiol. 40:2153-2162.[Abstract/Free Full Text]
  9. Sanders, C. C., W. E. Sanders, Jr., and E. S. Moland. 1986. Characterization of ß-lactamases in situ on polyacrylamide gels. Antimicrob. Agents Chemother. 30:951-952.[Abstract/Free Full Text]
  10. Tenover, F. C., R. K. Kalsi, P. P. Williams, R. B. Carey, S. Stocker, D. Lonsway, J. K. Rasheed, J. W. Biddle, J. E. McGowan, Jr., and B. Hanna. 2006. Carbapenem resistance in Klebsiella pneumoniae not detected by automated susceptibility testing. Emerg. Infect. Dis. 12:1209-1213.[Medline]
Ellen Smith Moland
Seong Geun Hong
Kenneth S. Thomson
Department of Medical Microbiology and Immunology
Center for Research in Anti-Infectives and Biotechnology
Creighton University School of Medicine
Omaha, Nebraska,1

Davise H. Larone
Department of Pathology and Laboratory Medicine
Weill Cornell Medical Center
New York-Presbyterian Hospital
New York, New York,2

Nancy D. Hanson*
Department of Medical Microbiology and Immunology
Center for Research in Anti-Infectives and Biotechnology
2500 California Plaza
Creighton University School of Medicine
Omaha, Nebraska 68178,3

* Phone: (402) 280-5837, Fax: (402) 280-1875, E-mail: ndhanson{at}creighton.edu

Antimicrobial Agents and Chemotherapy, February 2007, p. 800-801, Vol. 51, No. 2
0066-4804/07/$08.00+0     doi:10.1128/AAC.01143-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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