Outbreak of extended-spectrum β-lactamase producing Serratia marcescens in an intensive care unit

Abstract

Serratia marcescens has recently been identified as an important etiological agent in nosocomial infections, and is considered to be an opportunistic pathogen agent in immunosuppressed patients undergoing long periods of intensive care. Research carried out in 1991 and 1992 showed that it was of epidemiological relevance in only 1-% of clinical isolates at the Ospedale di Circolo, Varese, Italy. However, between 7 February and 11 October 1993, the incidence of cases attributable to S. marcescens had increased to 5%: 157 strains of Serratia marcescens were isolated from clinical specimens of 43 patients admitted to an intensive care unit; these strains, characterized by epidemic spread, showed the same pattern of multiresistance to antibiotics including monobactams and oxyimino-cephalosporins. During the same period 23 isolates were also recovered from 18 patients admitted to wards other than the intensive care unit; these strains, characterized by a wide range of antibiotic susceptibility, were also sensitive to β-lactam antibiotics with the exception of first generation cephalosporins. The production of extended-spectrum β-lactamases (ESβLs) and their genetic determinism were studied. All the epidemic strains of S. marcescens resistant to ceftazidime, cefotaxime, ceftriaxone and aztreonam produced three different β-lactamases with pI 5.4, 5.5 and 8.4 respectively. In contrast, non-epidemic strains produced only a β-lactamase with pI 8.4. The β-lactamase with pI 5.5 was plasmid-mediated, hydrolizing ceftazidime and aztreonam, showing it to be an ESβL; while the β-lactamase with pI 5.4, although plasmid-mediated, did not hydrolize monobactams or oxyimino-cephalosporins. The β-lactamase with pI 8.4 was found to be an inducible chromosomal enzyme capable of hydrolizing cefotaxime and ceftriaxone. Electrophoresis of the plasmid DNA indicated the presence of a similar plasmid of approximate size 54 kb in the resistant epidemic strains; this was found to be conjugative and mediating resistance also to aminoglycosides. Our data indicate that the plasmid-mediated production of ESβLs may contribute to the epidemic spread of Serratia marcescens in high-risk wards. © 1994.