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Characterization and mobilization of nonconjugative plasmids encoding resistance to streptomycin and sulfanilamide

Y Araki1, M Inoue, H Hashimoto

  • 1Laboratory of Drug Resistance in Bacteria, Gunma University School of Medicine.

Insights

Most clinical streptomycin (Sm) and sulfanilamide (Su) resistance in Enterobacteriaceae and Pseudomonas is linked to nonconjugative Inc Q plasmids. These plasmids are mobilized by other plasmids, explaining the widespread occurrence of resistant strains.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Genetics

Background:

  • Antibiotic resistance is a growing global health concern.
  • Nonconjugative plasmids play a significant role in the dissemination of antibiotic resistance genes.
  • Understanding plasmid mobility is crucial for controlling the spread of resistance.

Purpose of the Study:

  • To investigate the genetic basis of streptomycin (Sm) and sulfanilamide (Su) resistance in clinical isolates.
  • To determine the role of Inc Q plasmids in encoding SmSu resistance.
  • To analyze the mobilization and transferability of Inc Q plasmids within Enterobacteriaceae and Pseudomonas.

Main Methods:

  • Plasmid analysis of clinical isolates.
  • Conjugation experiments using various Inc P, Inc I, and Inc F group plasmids.
  • Mobilization assays to assess Inc Q plasmid transfer frequencies.
  • Characterization of transconjugant resistance and transferability.

Main Results:

  • Most nonconjugative Sm and Su resistance in clinical Enterobacteriaceae and Pseudomonas isolates was encoded by a 5.5 Md Inc Q plasmid.
  • Inc P plasmids efficiently mobilized the Inc Q plasmids between E. coli strains.
  • Inc I and Inc F plasmids showed lower efficiencies in mobilizing Inc Q plasmids.
  • High-frequency mobilization of Inc Q plasmids to Enterobacteriaceae occurred without the conjugative Inc P plasmid, resulting in nontransferable SmSu-resistant transconjugants.

Conclusions:

  • Inc Q plasmids are a major vehicle for nonconjugative SmSu resistance in clinical settings.
  • The efficient mobilization of Inc Q plasmids by other plasmid groups facilitates their spread.
  • The generation of nontransferable resistant strains through mobilization can explain their wide distribution among clinical isolates.

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