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Chromosomal origin of acetyltransferase AAC(6') specifying amikacin resistance in Serratia marcescens
R Gómez-Lus1, M J Rivera, D Bobey
1Department of Microbiology, School of Medicine, Zaragoza, Spain.
Abstract:
Two clinical isolates of Serratia marcescens resistant to aminoglycoside-aminocyclitols and other antibiotics have been examined for aminoglycoside-modifying enzymes. Both strains were amikacin-resistant, and this resistance was mediated by an acetyltransferase AAC(6'). S. marcescens 737 contains a single conjugative plasmid, pUZ 737, of 135 kilobases, which confers resistance to gentamicin and tobramycin by a nucleotidyltransferase, ANT(2"), and to kanamycin, neomycin, butirosin and lividomycin by a phosphotransferase, APH(3'). S. marcescens 1830 does not contain extrachromosomal DNA, and it produced only the above mentioned AAC(6'). The presence of AAC(6') and associated aminoglycoside resistance are not dependent on the presence of a detectable plasmid, not transferred by conjugation, and not cured. Therefore, this enzyme is probably encoded by a chromosomal gene.
Insights
Two Serratia marcescens strains exhibit antibiotic resistance. One strain
Area of Science:
- Microbiology
- Molecular Biology
- Genetics
Background:
- Clinical isolates of Serratia marcescens can develop resistance to multiple antibiotics, including aminoglycosides.
- Aminoglycoside resistance is often mediated by aminoglycoside-modifying enzymes.
Purpose of the Study:
- To investigate the aminoglycoside-modifying enzymes present in two clinical isolates of Serratia marcescens exhibiting amikacin resistance.
- To determine the genetic basis of aminoglycoside resistance in these strains.
Main Methods:
- Phenotypic characterization of antibiotic resistance.
- Enzyme assays to identify aminoglycoside-modifying enzymes.
- Plasmid analysis and conjugation experiments.
Main Results:
- Both Serratia marcescens strains possessed an acetyltransferase AAC(6") conferring amikacin resistance.
- Strain 737 harbored a plasmid (pUZ 737) encoding a nucleotidyltransferase ANT(2") for gentamicin/tobramycin resistance and a phosphotransferase APH(3") for kanamycin/neomycin resistance.
- Strain 1830, lacking extrachromosomal DNA, only produced AAC(6"), suggesting chromosomal gene encoding.
Conclusions:
- Aminoglycoside resistance in Serratia marcescens can be mediated by both plasmid-borne and chromosomally encoded enzymes.
- The AAC(6") enzyme, conferring amikacin resistance, appears to be chromosomally encoded in strain 1830, independent of plasmid presence.