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Survey of modifying enzymes and plasmids in amikacin-resistant Serratia marcescens
Abstract:
Forty amikacin-resistant strains of Serratia marcescens isolated from four different hospitals (A, B, C, and D) were examined for modifying enzymes and plasmids. Twenty-one of the isolates produced acetyltransferase that modified amikacin. Eighteen of the 21 acetyltransferase-bearing isolates were from different inpatients in hospital A and the other three were from hospital C. Amikacin resistance was mediated by conjugative plasmid of 24 megadaltons in 15 of the 18 acetyltransferase-bearing isolates of hospital A and by nonconjugative plasmids, derivatives of the 24-megadalton plasmids, in the remaining three isolates of the same hospital. The 24-megadalton plasmid determined aminoglycoside acetyltransferase (6') IV. This plasmid-borne enzyme conferred amikacin resistance on S. marcescens but not on Escherichia coli K12. The frequency of transfer of the 24-megadalton plasmid from the S. marcescens isolate to E. coli K12 by conjugation was approximately 10(-7) (transconjugants/donors) and was 0.1% of that between E. coli strains. In acetyltransferase-bearing isolates from hospital C, the enzyme was mediated by a nonconjugative plasmid in one case and could not be associated with a plasmid in the remaining two cases. Neither enzymes nor plasmids could be associated with amikacin resistance of the isolates of the other two hospitals.
Insights
Amikacin resistance in Serratia marcescens is often due to acetyltransferase enzymes carried on plasmids. These plasmids can transfer resistance, posing a public health concern in hospitals.
Area of Science:
- Microbiology
- Molecular Biology
- Infectious Diseases
Background:
- Amikacin is a crucial antibiotic for treating serious Gram-negative bacterial infections.
- Emergence of amikacin-resistant bacteria, like Serratia marcescens, is a growing global health threat.
- Understanding resistance mechanisms is vital for effective infection control and treatment strategies.
Purpose of the Study:
- To investigate the genetic basis of amikacin resistance in Serratia marcescens strains.
- To identify the role of modifying enzymes and plasmids in conferring amikacin resistance.
- To assess the transmissibility of amikacin resistance genes between bacterial strains.
Main Methods:
- Isolation and characterization of amikacin-resistant Serratia marcescens from hospital settings.
- Enzyme assays to detect amikacin-modifying enzymes, specifically acetyltransferases.
- Plasmid analysis, including conjugation experiments and molecular characterization of resistance plasmids.
Main Results:
- Twenty-one of forty amikacin-resistant Serratia marcescens strains produced amikacin-modifying acetyltransferase.
- Amikacin resistance in most hospital A isolates was mediated by a 24-megadalton conjugative plasmid encoding aminoglycoside acetyltransferase (6') IV.
- Plasmid-mediated resistance was observed in some hospital C isolates, but not in isolates from hospitals B and D.
Conclusions:
- Plasmid-borne aminoglycoside acetyltransferase (6') IV is a significant mechanism of amikacin resistance in Serratia marcescens.
- The conjugative nature of the resistance plasmid facilitates its spread within and potentially between bacterial populations.
- Hospital-specific resistance patterns highlight the need for targeted surveillance and control measures.