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Streptomycin and Spectinomycin resistance mediated by plasmids.
Antimicrobial Agents and Chemotherapy
|June 1, 1978
Summary
Streptomycin resistance in E. coli and Shigella clinical isolates is often due to nonconjugative plasmids. Resistance mechanisms involve drug inactivation via adenylylation or phosphorylation.
Area of Science:
- Microbiology
- Molecular Biology
- Antimicrobial Resistance
Background:
- Antimicrobial resistance is a growing global health concern.
- Escherichia coli and Shigella are common causes of bacterial infections.
- Understanding resistance mechanisms is crucial for effective treatment.
Purpose of the Study:
- To investigate the prevalence and mechanisms of resistance to tetracycline, chloramphenicol, streptomycin, and sulfanilamide.
- To differentiate between conjugative and nonconjugative resistance plasmids.
- To elucidate the biochemical basis of streptomycin resistance.
Main Methods:
- Survey of clinical isolates of Escherichia coli and Shigella.
- Plasmid analysis to determine conjugative and nonconjugative types.
- Biochemical assays to determine streptomycin resistance mechanisms (adenylylation and phosphorylation).
Main Results:
- Nonconjugative streptomycin and sulfanilamide-resistant plasmids were more frequent than conjugative R plasmids.
- Streptomycin resistance was mediated by adenylylation in some conjugative plasmids.
- Phosphorylation was the mechanism for streptomycin inactivation in other conjugative and all nonconjugative plasmids.
Conclusions:
- Nonconjugative plasmids play a significant role in streptomycin and sulfanilamide resistance in clinical E. coli and Shigella.
- Multiple biochemical mechanisms contribute to streptomycin resistance, highlighting the adaptability of these bacteria.