SME-2-Producing Serratia marcescens Isolate from Switzerland

Antimicrobial Agents and Chemotherapy
2007.0

Abstract

Carbapenemases in Serratia marcescens have been rarely reported, being related either to metallo-β-lactamases IMP-1, IMP-6, and VIM-2 or to SME-type Ambler class A β-lactamases. SME-1 was first identified from the carbapenem-resistant S. marcescens strain S6 isolated in London in 1982, then in carbapenem-resistant S. marcescens strains from the United States in 1999. It hydrolyzes penicillins, aztreonam, cephalosporins, and carbapenems and is inhibited by clavulanic acid, with the blaSME-1 gene chromosome encoded in isolate S6. The SME-2 and SME-3 variants have been identified from S. marcescens isolates recovered from the United States and United Kingdom. Our study was initiated by the isolation in May 2006 at the University Hospital of Lausanne, Switzerland, of a carbapenem-resistant S. marcescens isolate from an exudate obtained after a parotidectomy of a 62-year-old patient who received amoxicillin-clavulanate prophylaxis and later imipenem for pulmonary deficiency. Strain AW was resistant to penicillins and imipenem, with MICs of imipenem, meropenem, and ertapenem being 32, 8, and 4 μg/ml, respectively; it was also resistant to cefoxitin and aztreonam but susceptible to expanded-spectrum cephalosporins. Double-disk synergy testing indicated production of a carbapenemase inhibited by clavulanic acid. PCR amplification and sequencing identified a gene encoding SME-2. Pulsed-field gel electrophoresis showed isolate AW was not clonally related to isolate S6. rpoB gene sequence analysis ruled out a possible subspecies identity for SME producers. Conjugation, electrotransformation, and plasmid analysis suggested a chromosomal location for the blaSME-2 gene, with the LysR-type regulatory gene smeR upstream of blaSME-2. This report underlines the possible worldwide identification of SME-type S. marcescens producers. Along with other clavulanic acid-inhibited carbapenemases (NMC-A, IMI, KPC), SME-type enzymes may confer clinically significant resistance to carbapenems, and SME producers may have a lower level of resistance to ertapenem than to other carbapenems.

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