Carbapenem-resistant Serratia marcescens isolates producing Bush
Group 2f -lactamase (SME-1) in the United States: Results from the
MYSTIC Programme
Ana C. Gales
a
, Douglas J. Biedenbach
a,c
, Patricia Winokur
b
, Donna M. Hacek
d
,
Michael A. Pfaller
a,c
, Ronald N. Jones
a,c,
*
a
Department of Pathology, University of Iowa College of Medicine, Iowa City, Iowa
b
Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, Iowa
c
CAST Laboratories, Iowa City, Iowa
d
Departments of Medicine and Pathology, Northwestern University, Chicago, Illinois
Received 30 October 2000; accepted 15 November 2000
Abstract
Two carbapenem (imipenem, meropenem)-resistant Serratia marcescens strains were isolated in the United States (Chicago, IL) through
the 1999 MYSTIC (Meropenem Yearly Susceptibility Test Information Collection) Programme. The S. marcescens antimicrobial suscep-
tible patterns were: susceptible to ceftriaxone, ceftazidime, and cefepime (MICs, 0.25 g/ml), and resistance to the carbapenems
(imipenem and meropenem; MIC, 32 g/ml) and aztreonam (MIC, 16 g/ml). Each S. marcescens isolate shared an identical
epidemiologic type (ribotype and PFGE) and the outer membrane protein profile was also identical to those of the wild type susceptible
strains from the same medical center. The PCR utilizing bla
sme-1
primers amplified a gene product that was identified as consistent with
SME-1 after DNA sequencing. Imipenem and meropenem resistance due to production of carbapenem-hydrolyzing enzymes among clinical
isolates is still very rare, but microbiology laboratories should be aware of these chromosomally encoded enzymes among class C
-lactamases producing enteric bacilli such as S. marcescens and Enterobacter cloacae. © 2001 Elsevier Science Inc. All rights reserved.
1. Introduction
Serratia marcescens has become an important nosoco-
mial organism acting as an opportunistic pathogen to cause
diverse types of serious infections (Hejazi & Falkiner,
1997). The therapeutic use of -lactams for infections
caused by S. marcescens can be limited due to production of
chromosomal class C -lactamases that are generally induc-
ible, but may become stably derepressed thus producing
additional resistance to some broad-spectrum cephalospo-
rins (Jones, 1998). Resistance to newer cephalosporins
among S. marcescens isolates has also been reported sec-
ondary to the production of class A extended-spectrum
-lactamases (ESBL) (Kunugita et al., 1995), and when
resistance to these cephalosporins emerges (either due to an
ESBL or elevated class C -lactamase production), the
carbapenems have been treatment options (Jones, 1998).
Among the Enterobacteriaceae, the rare occurrences of
carbapenem resistances arise via two mechanisms: 1) high
level production of class C chromosomal cephalosporinase
combined with altered outer membrane permeability de-
scribed in S. marcescens, Enterobacter cloacae, Enter-
obacter aerogenes, and Providencia rettgeri isolates (Jones,
1998; Weindorf et al., 1998); and 2) resistance resulting
from the synthesis of -lactamases capable of hydrolyzing
carbapenems (Ito et al., 1995; Rasmussen & Bush, 1997;
Yang et al., 1990). Resistance to carbapenems due to car-
bapenem-hydrolyzing enzymes has been described in S.
marcescens isolates in the United States (US) and Europe
(Queenan et al., 2000; Yang et al., 1990). In contrast,
emergence of carbapenem resistance in Japan among S.
marcescens has reached a prevalence of 3.8% in certain
areas, where dissemination of a plasmid mediated bla
imp
metallo--lactamase has occurred (Ito et al., 1995).
In this report, we describe the mechanism of resistance to
* Corresponding author. The Jones Group, 345 Beaver Kreek Center,
Suite A, North Liberty, IA 52317 Tel.: +1-319-665-3370; fax: +1-319-
665-3371.
E-mail address: ronald-jones@jonesgr.com. (R.N. Jones).
www.elsevier.com/locate/diagmicrobio
Diagnostic Microbiology and Infectious Disease
39 (2001) 125–127
0732-8893/01/$ – see front matter © 2001 Elsevier Science Inc. All rights reserved.
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