Mechanisms of resistance to piperacillin of Enterobacter cloacae strains differ by antibiotic prescription policy.

During a study of piperacillin resistance among aerobic Gram-negative bacteria, 18 resistant strains of Enterobacter cloacae were obtained from a General Hospital in Rotterdam and 13 from a University Hospital in Amsterdam. The patterns of antibiotic susceptibilities were different: the Amsterdam strains were generally resistant to penicillins, the third generation cephalosporins and temocillin, whereas the Rotterdam strains were more often sensitive to the third generation cephalosporins and temocillin but more resistant to penicillins. Isoelectric focusing and substrate profiles showed the presence of chromosomal Class 1 beta-lactamase in ten of the Amsterdam strains: in three strains a plasmid mediated TEM-1 enzyme was detected. In contrast 15 of the 18 Rotterdam strains possessed a plasmid mediated beta-lactamase, ten of which were TEM-2. Eight of the ten strains with the TEM-2 enzyme harboured a transferable plasmid coding for resistance to piperacillin. Endonuclease analysis of plasmid DNA from these eight strains revealed an identical pattern in seven strains. Different selective pressures were operative in each hospital. In Amsterdam the general use of cefotaxim and piperacillin favoured emergence of strains with derepressed chromosomal Class 1 beta-lactamase, whereas in Rotterdam the use of cefuroxime favoured the spread of a plasmid, encoding TEM-2 beta-lactamase.