Properties of R plasmids determining gentamicin resistance by acetylation in Pseudomonas aeruginosa
Abstract:
Two clinical isolates of Pseudomonas aeruginosa, one a pyocin type 5 strain from Atlanta, could transfer gentamicin resistance by conjugation. Donor and recipient strains inactivated gentamicin by acetylation. The R plasmids, pMG1 and pMG2, also determined resistance to sisomicin, another substrate of gentamicin acetyltransferase I, sulfonamides, and streptomycin, but not resistance to kanamycin, neomycin, tobramycin, butirosin, or BB-K 8. They were transmissible to many strains of P. aeruginosa, including a Rec(-) strain, but not to Escherichia coli or other enterobacteriaceae. These R plasmids were compatible with R plasmids transmissible to P. aeruginosa from E. coli, including members of C, N, P, and W incompatibility groups. From a strain carrying pMG1 and a compatible plasmid, pMG1 was transferred independently but transfer of the second plasmid often resulted in cotransfer of pMG1. In contrast, pMG1 and pMG2 were incompatible with pseudomonas R plasmids R931 and R3108, and with R931 they readily formed recombinant plasmids. The four plasmids in this incompatibility group determine additional biological properties, including resistance to inorganic and organic mercury compounds, to ultraviolet light, and to certain deoxyribonucleic acid phages. pMG1 and pMG2 also phenotypically inhibited pyocin production. Consequently such R plasmids alter the phage and pyocin types of their host strains.
Insights
Two Pseudomonas aeruginosa strains transferred gentamicin resistance via plasmids pMG1 and pMG2. These R plasmids conferred resistance to sisomicin, sulfonamides, and streptomycin, altering host pyocin and phage types.
Area of Science:
- Microbiology
- Genetics
- Molecular Biology
Background:
- Pseudomonas aeruginosa is an opportunistic pathogen.
- Antibiotic resistance in bacteria is a growing public health concern.
- R plasmids mediate antibiotic resistance transfer between bacteria.
Purpose of the Study:
- To characterize the R plasmids responsible for gentamicin resistance transfer in clinical isolates of P. aeruginosa.
- To determine the genetic basis and transferability of these R plasmids.
- To investigate the incompatibility and recombination properties of these R plasmids.
Main Methods:
- Conjugation experiments were performed to transfer gentamicin resistance.
- Acetylation assays were used to determine the mechanism of gentamicin inactivation.
- Plasmid incompatibility and restriction mapping were employed to analyze plasmid relationships.
- Phage and pyocin typing were conducted to assess phenotypic changes.
Main Results:
- Two R plasmids, pMG1 and pMG2, were identified and transferred via conjugation.
- These plasmids conferred resistance to gentamicin, sisomicin, sulfonamides, and streptomycin.
- The plasmids were transferable to P. aeruginosa but not to enterobacteriaceae.
- pMG1 and pMG2 were incompatible with certain Pseudomonas R plasmids and formed recombinants with R931.
- The R plasmids also conferred resistance to mercury, UV light, and altered pyocin and phage types.
Conclusions:
- R plasmids pMG1 and pMG2 are important vehicles for the spread of antibiotic resistance in P. aeruginosa.
- These plasmids carry a broad range of resistance genes and influence bacterial phenotype.
- Understanding R plasmid dynamics is crucial for combating antibiotic resistance in clinical settings.
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