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Outbreak of extended-spectrum beta-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 1-2% 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 beta-lactam antibiotics with the exception of first generation cephalosporins. The production of extended-spectrum beta-lactamases (ES beta Ls) and their genetic determinism were studied. All the epidemic strains of S. marcescens resistant to ceftazidime, cefotaxime, ceftriaxone and aztreonam produced three different beta-lactamases with pI 5.4, 5.5 and 8.4 respectively. In contrast, non-epidemic strains produced only a beta-lactamase with pI 8.4. The beta-lactamase with pI 5.5 was plasmid-mediated, hydrolizing ceftazidime and aztreonam, showing it to be an ES beta L; while the beta-lactamase with pI 5.4, although plasmid-mediated, did not hydrolize monobactams or oxyimino-cephalosporins.(ABSTRACT TRUNCATED AT 250 WORDS)
Insights
Serratia marcescens infections increased in an Italian ICU, with epidemic strains showing multi-drug resistance. These resistant strains produced specific extended-spectrum beta-lactamases (ESBLs), indicating a significant rise in nosocomial pathogens.
Area of Science:
- Medical Microbiology
- Infectious Diseases
- Antimicrobial Resistance
Background:
- Serratia marcescens is an opportunistic pathogen causing nosocomial infections, particularly in intensive care units.
- Previous studies (1991-1992) indicated low epidemiological relevance (1-2%) of S. marcescens in clinical isolates.
- A significant increase in S. marcescens incidence (to 5%) was observed between February and October 1993.
Purpose of the Study:
- To investigate the increased incidence of Serratia marcescens in a hospital setting.
- To characterize the antibiotic resistance patterns of S. marcescens isolates.
- To study the production and genetic basis of extended-spectrum beta-lactamases (ESBLs) in epidemic strains.
Main Methods:
- Isolation and characterization of 157 S. marcescens strains from intensive care unit patients and 23 strains from other wards.
- Antibiotic susceptibility testing, focusing on resistance to monobactams and oxyimino-cephalosporins.
- Analysis of beta-lactamase production, including isoelectric focusing (pI) and plasmid mediation.
Main Results:
- Epidemic S. marcescens strains from the ICU exhibited multi-drug resistance, including to monobactams and oxyimino-cephalosporins.
- Non-epidemic strains showed broader antibiotic susceptibility, with exceptions for first-generation cephalosporins.
- Epidemic strains produced three beta-lactamases (pI 5.4, 5.5, 8.4), with the pI 5.5 enzyme identified as an ESBL hydrolyzing ceftazidime and aztreonam.
- Non-epidemic strains produced only a beta-lactamase with pI 8.4.
Conclusions:
- The study highlights a concerning rise in multi-drug resistant Serratia marcescens in an intensive care unit.
- The emergence of plasmid-mediated extended-spectrum beta-lactamases (ESBLs) in epidemic strains is a key factor in their resistance.
- These findings underscore the need for vigilant surveillance and control measures against nosocomial infections caused by resistant pathogens.