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beta-Lactam resistance amongst Enterobacter species
1Department of Medical Microbiology, Creighton University School of Medicine, Omaha, Nebraska 68178.
The Journal of Antimicrobial Chemotherapy
|November 1, 1993
Summary
Enterobacter species rapidly develop resistance to newer cephalosporins due to a chromosomal cephalosporinase enzyme. This beta-lactam resistance mechanism is driven by increased antibiotic use, necessitating judicious prescribing and new drug development.
Area of Science:
- Microbiology
- Pharmacology
- Infectious Diseases
Background:
- Enterobacter species prevalence increased with extended-spectrum cephalosporin use.
- These bacteria possess natural resistance to older cephalosporins and rapidly acquire resistance to newer agents.
- Bush group 1 chromosomal cephalosporinase is the primary mechanism for beta-lactam resistance in Enterobacter.
Purpose of the Study:
- To explain the mechanisms of beta-lactam resistance in Enterobacter species.
- To investigate the link between cephalosporin use and the rise of resistant strains.
- To explore strategies for combating emerging antibiotic resistance.
Main Methods:
- Review of existing literature on Enterobacter resistance mechanisms.
- Analysis of surveys on multi-drug resistant Enterobacter prevalence.
- Examination of enzyme kinetics and drug penetration factors.
Main Results:
- Resistance is mediated by an inducible chromosomal cephalosporinase (Bush group 1).
- Mutants overexpressing this enzyme confer resistance to newer cephalosporins, penicillins, and monobactams.
- Increased use of newer cephalosporins correlates with higher prevalence of resistant Enterobacter strains.
Conclusions:
- Enterobacter's resistance mechanism involves high-affinity cephalosporinase and poor drug penetration.
- Judicious use of current beta-lactams and development of novel cephalosporins are key strategies.
- Newer cephalosporins with lower enzyme affinity and faster cell penetration show promise in overcoming resistance.