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PubMed1989

The emergence of beta-lactam resistance among strains of Enterobacter cloacae and Pseudomonas aeruginosa.

The development of multiresistant bacterial strains associated with the use of the new beta-lactam antibiotic agents has prompted investigation into the mechanisms involved. Factors influencing beta-lactamase production, alterations of target-protein structure or production and decreases in bacterial outer membrane permeability have been identified as the three general mechanisms of beta-lactam resistance in aerobic Gram-negative bacteria. Because there is no DNA interaction by beta-lactam agents, emergence of resistance results from either spontaneous mutation or the presence of resistant subpopulations; the presence of antibiotics allows for overgrowth of resistant strains. Studies have indicated that there is a significant relationship between the rate of emerging resistance and the ratio of the minimum inhibitory concentration of a beta-lactam to the drug concentration used to select for resistance in vitro or achieved at the infection site in vivo. It is concluded that the use of synergistic combinations of agents should reduce the emergence of beta-lactam-resistant bacterial strains. Thus the choice of an appropriate therapeutic agent requires thorough evaluation of the specific pathogen for susceptibility to a variety of beta-lactam agents and aminoglycosides.

Animals↗
PubMed1996

Investigation of outbreaks of Enterobacter aerogenes colonisation and infection in intensive care units by random amplification of polymorphic DNA.

During a 4-month period, 41 isolates of Enterobactor aerogenes were cultured from different specimens from a 14-bed intensive care unit (ICU1). These were obtained from 12 patients out of a total of 187 patients admitted to the ICU. Sixteen E. aerogenes isolates were cultured from another ICU (ICU2) 6 months later. Six non-outbreaks associated strains were included as controls and all the isolates were compared by random amplification of polymorphic DNA (RAPD), with three different 10-mer oligonucleotide primers. RAPD fingerprinting with primer AP12h was as discriminatory as the combined results from all three primers and defined 22 different patterns for the 41 isolates from the ICU1. In nine instances, isolates with indistinguishable RAPD patterns were detected in two-to-five patients over a 3-15-day period, suggesting patient-to-patient transmission. During their stay in ICU1, patients harboured one-to-12 distinguishable isolates. Isolates from ICU2 were indistinguishable by RAPD analysis with the three different primers. These findings suggest that the cluster of colonisations and infections in ICU1 was a 'false outbreak', consisting of successive patient-to-patient transmission of different E. aerogenes strains. In contrast, the outbreak on ICU2 probably involved the extensive spread of a single strain.

Adult↗
PubMed1984

Beta-lactamase production in Enterobacter cloacae and Citrobacter freundii.

The beta-lactamase activity with ampicillin (A) and cephalothin (Ce) as substrate was examined in 28 strains of Ent. cloacae and 24 strains of C. freundii by a micro-iodometric-(MIA) and an ultraviolet assay (UVA). Carbenicillin resistance (Ca-R) was present in 32 strains (16 of each species). All Ca-resistant (Ca-r) strains had elevated amounts of beta-lactamase. The conditions were very similar in the two species. The Ca-r strains could be divided into two subgroups. One group had very high ampicillinase activity and lower cephalothinase activity in MIA. In UVA the cephalothinase activity was equal to that in MIA. The strains could transfer their A- and Ca-R. The reaction velocity increased with time in MIA. The Ca-R was probably plasmid mediated. The other group had no or low ampicillinase activity in MIA. The cephalothinase activity in UVA was much higher than in MIA. Velocity decreased with time in MIA, probably due to inhibition by iodine. The strains were very Ce-r and could not transfer A-R. The Ca- and Ce-R was probably chromosomally mediated. The acquisition of Ca-R in Ent. cloacae and C. freundii was analogous to acquisition of A-R in E. coli. The fraction of strains with high ampicillinase activity (plasmid mediated among all strains with acquired beta-lactam resistance was the same in Ent. cloacae and C. freundii, viz. 0.63. In E. coli the corresponding value is 0.61. This fraction thus seems rather constant between the different genera.

Ampicillin↗
PubMed2000

Role of penicillin-binding proteins in the initiation of the AmpC beta-lactamase expression in Enterobacter cloacae.

Penicillin-binding proteins (PBPs) are involved in the regulation of beta-lactamase expression by determining the level of anhydromuramylpeptides in the periplasmatic space. It was hypothesized that one or more PBPs act as a sensor in the beta-lactamase induction pathway. We have performed induction studies with Escherichia coli mutants lacking one to four PBPs with DD-carboxypeptidase activity. Therefore, we conclude that a strong beta-lactamase inducer must inhibit all DD-carboxypeptidases as well as the essential PBPs 1a, 1b, and/or 2.

Bacterial Proteins↗