Further occurrence of extended-spectrum beta-lactamase-producing Salmonella enteritidis.

We describe the further occurrence of Salmonella enteritidis producing an extended spectrum beta-lactamase (ESBL) and transferring cefotaxime, ceftazidime and aztreonam resistance. In a previous communication we describe the isolation of a strain of S. enteritidis (No. 35) from a septic neonate with high-level resistance to cefuroxime, cefotaxime, ceftazidime and aztreonam. Six weeks later, a second neonate was found, in the same Pediatric University Hospital, to be infected with apparently the same strain of S. enteritidis (No. 100) which was isolated from blood with similar properties as the strain No. 35. In this strain we were able to study, in more detail, the transferability of its resistance to 3rd generation cephalosporins and its ESBL production. In this report we describe results of transfer experiments, relative rates of hydrolysis (Vmax) and ESBL tests which indicate that the capacity to produce ESBL was transferred from the multiply-resistant strain of S. enteritidis No. 100 to S. typhimurium LT-2 rif+str+.

Mobilization of antibiotic resistance for transfer in Pseudomonas aeruginosa.

We describe a phenomenon of mobilization of antibiotic resistance from non-transferring strains of Pseudomonas aeruginosa by cultivation with strains of P.aeruginosa capable of transferring determinants of antibiotic resistance to a susceptible recipient strain by triparental cross. In this report we described two strains of P.aeruginosa capable to mobilize for transfer the resistance determinants in strains of P.aeruginosa with multiply antibiotic resistance which were not themselves transferable to Pseudomonas recipient strains. Two strains of P.aeruginosa No. 282 and 283 from Bata's Hospital in Zlín, Czech Republic, were used as donor strains for experiments in triparental crosses. They were resistant to carbenicillin (CAR), kanamycin (KAN), cefalotin-cefazolin (CFR), cefotaxime (CTX), ceftazidime (CAZ) and aztreonam (AZA). Both strains transferred CFR resistance to Escherichia coli K-12 rif+ recipient, but not to P.aeruginosa PAO recipients. In a second system, a strain of P.aeruginosa No. 76 from Frankfurt University Clinics was used as a donor strain. It transfers CAR resistance to PAO-1670 rif+, but not to E. coli K-12 rif+. Two strains of P.aeruginosa from Frankfurt University Clinics No. 76 and 229 were used as intermediary recipient strains. They were resistant to CAR, KAN, CTX, CAZ, AZA, imipenem (IMP) and ofloxacin (OFL). Strain No. 229 did not transfer any antibiotic resistance to any of both final recipient strains. Strain No. 76 transfers, as indicated, CAR resistance determinant to PAO 1670 rif+ recipient strain. Strains of E. coli K-12 No. 3110 rif+ and P.aeruginosa PAO 1670 rif+ were used as final recipient strains.

The origin, by mutation, of high level resistance to ceftazidime and cefotaxime in a clinical isolate of Enterobacter cloacae.

Although strains of Enterobacter sp. produce a chromosomal AmpC beta-lactamase, they have been, in general, susceptible to cefotaxime or ceftazidime. But now resistance to ceftazidime has increased in nosocomial Enterobacter strains, reaching the level of 40%. A chromosomal mutation in the amp operon coding the production of AmpC type beta-lactamase may cause a change in the conversion of a susceptible strain of Enterobacter to a highly resistant mutant. The production of AmpC enzyme is inducible and third-generation cephalosporins are weak inducers of AmpC production. Spontaneous mutations (or insertions of transposons) in the regulatory region of amp operon might create constitutive (derepressed) overproducers of large amounts of AmpC molecules. As a consequence, such cells acquire a stable resistance to beta-lactam antibiotics including cefotaxime or ceftazidime. We describe the origin of mutants of a clinical isolate of Enterobacter cloacae that acquired high-level resistance to ceftazidime followed by the resistance to cefotaxime and/or aztreonam due to a second mutation.

A bi-modal transfer of antibiotic resistance by conjugation and transduction from an imipenem-resistant strain of Pseudomonas aeruginosa.

A strain of Pseudomonas aeruginosa No. 76/17224 resistant to carbenicillin (CAR), kanamycin (KAN), cefalotin (CLO), cefotaxime (CTX), ceftazidime (CAZ), aztreonam (AZA), imipenem (IMI) and ofloxacin (OFL) was isolated at the Frankfurt University Hospital. This strain transferred, by conjugation, antibiotic resistance determinants to CAR, CLO, CTX, CAZ and AZA. In addition, we isolated a wild-type phage from this strain. We used this phage to transduce the resistance determinants to four susceptible recipient strains of P. aeruginosa. The phage designated AP-76 transduced the resistance determinants to KAN, CAR, CTX and CAZ to all four recipient strains. Imipenem and aztreonam resistance determinants were directly transduced to two recipient strains only, i.e. to PAO-1670 and ML-1008. The IMI resistance determinant was not co-transduced with any other resistance determinant(s) selected directly. Our results indicated that IMI resistance determinant was not associated with other resistance determinants. IMI was actively hydrolysed by IMI-resistant transductants and this hydrolysis was inhibited by clavulanate but not by EDTA.