MECHANISMS OF RESISTANCE TO PIPERACILLIN OF ENTEROBACTER-CLOACAE STRAINS DIFFER BY ANTIBIOTIC PRESCRIPTION POLICY

Citation
F. Namavar et al., MECHANISMS OF RESISTANCE TO PIPERACILLIN OF ENTEROBACTER-CLOACAE STRAINS DIFFER BY ANTIBIOTIC PRESCRIPTION POLICY, International journal of antimicrobial agents, 8(3), 1997, pp. 205-208
Citations number
8
Categorie Soggetti
Microbiology,"Pharmacology & Pharmacy
ISSN journal
09248579
Volume
8
Issue
3
Year of publication
1997
Pages
205 - 208
Database
ISI
SICI code
0924-8579(1997)8:3<205:MORTPO>2.0.ZU;2-T
Abstract
During a study of piperacillin resistance among aerobic Gram-negative bacteria, 18 resistant strains of Enterobacter cloacae were obtained f rom a General Hospital in Rotterdam and 13 from a University Hospital in Amsterdam. The patterns of antibiotic susceptibilities were differe nt; 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 cephalospor ins and temocillin but more resistant to penicillins. Isoelectric focu sing and substrate profiles showed the presence of chromosomal Class 1 beta-lactamase in ten of the Amsterdam strains: in three strains a pl asmid mediated TEM-1 enzyme was detected. In contrast 15 of the 18 Rot terdam strains possessed a plasmid mediated beta-lactamase, ten of whi ch were TEM-2. Eight of the ten strains with the TEM-2 enzyme harboure d a transferable plasmid coding for resistance to piperacillin. Endonu clease analysis of plasmid DNA from these eight strains revealed an id entical pattern in seven strains. Different selective pressures were o perative in each hospital. In Amsterdam the general use of cefotaxim a nd piperacillin favoured emergence of strains with derepressed chromos omal Class 1 beta-lactamase, whereas in Rotterdam the use of cefuroxim e favoured the spread of a plasmid, encoding TEM-2 beta-lactamase. (C) 1997 Elsevier Science B.V.