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We studied antibiotic resistance patterns and extended-spectrum beta-lactamases (ES beta Ls) production in Serratia marcescens strains isolated in our hospital during 1993. We examined 210 S. marcescens isolates. Of these, 172 were obtained from 49 patients admitted to an intensive care ward; 157 out of 172 were obtained from February to October and presented the same pattern of antibiotic resistance, including monobactams and oxyimino-cephalosporins. The remaining 15 out of 172 isolates (obtained from September to December) were susceptible to all drugs tested, with the exception of first generation cephalosporins. Thirty-eight additional isolates were recovered, during the same period, from 28 patients admitted to wards other than the intensive care unit; also these strains showed the high susceptibility pattern reported above. Epidemic strains of S. marcescens produced three different types of beta-lactamase with pI 5.4, 5.5, and 8.4. In contrast, non-epidemic strains produced only one type of beta-lactamase with pI 8.4. Conjugation experiments showed that the beta-lactamases having a pI of 5.4 and 5.5 (but not the one with pI 8.4) were plasmid-mediated. Since the beta-lactamase with pI 5.5 was capable of hydrolyzing monobactams and oxyimino-cephalosporins it was classified as ES beta L. Electrophoretic analysis showed that plasmids obtained from multiresistant strains were of about 54 kb; these plasmids appeared also to code for aminoglycoside resistance. Our data indicate that the plasmid-mediated production of ES beta Ls may contribute to the epidemic spread of Serratia marcescens in high-risk wards.
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