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[Pseudomonas aeruginosa plasmids that control streptomycin resistance]
Antibiotiki
|August 1, 1979
Summary
Streptomycin resistance is widespread in Pseudomonas aeruginosa clinical strains, often mediated by plasmids encoding inactivating enzymes. One plasmid, however, confers resistance through altered cell wall permeability.
Area of Science:
- Microbiology
- Molecular Biology
- Genetics
Background:
- Antibiotic resistance is a growing global health concern.
- Pseudomonas aeruginosa is an opportunistic pathogen frequently associated with hospital-acquired infections.
- Resistance plasmids play a crucial role in the dissemination of antibiotic resistance genes.
Purpose of the Study:
- To investigate the prevalence and characteristics of streptomycin resistance determinants in clinical isolates of Pseudomonas aeruginosa.
- To identify the genetic mechanisms underlying streptomycin resistance in these strains.
- To analyze the properties of resistance plasmids found in Pseudomonas aeruginosa.
Main Methods:
- Plasmid isolation and characterization from clinical Pseudomonas aeruginosa strains.
- Determination of plasmid incompatibility groups and transfer frequencies.
- Enzyme assays to detect streptomycin-inactivating mechanisms (phosphorylation, adenylation).
- Analysis of streptomycin resistance conferred by a specific plasmid (pBSII) potentially involving cell wall permeability changes.
Main Results:
- A high prevalence (83%) of streptomycin resistance determinants was found on plasmids in clinical Pseudomonas aeruginosa strains.
- Nine plasmids conferring resistance to streptomycin and other agents (antibiotics, metal ions, UV) were identified.
- Eight of the nine plasmids encoded streptomycin phosphotransferase, indicating phosphorylation as a common inactivation mechanism.
- Enzymes showed specificity for streptomycin and dihydrostreptomycin, with similar molecular weights (approx. 20,000).
- One plasmid (pBSII) conferred streptomycin resistance without detectable inactivating enzymes, suggesting altered cell wall permeability.
Conclusions:
- Streptomycin resistance in clinical Pseudomonas aeruginosa is largely plasmid-mediated and frequently involves enzymatic inactivation via phosphorylation.
- The diversity of resistance plasmids highlights the adaptability of Pseudomonas aeruginosa to antimicrobial agents.
- The identification of a novel resistance mechanism associated with plasmid pBSII warrants further investigation into bacterial cell wall modifications.