[Aminoglycoside modifying enzymes (author's transl)]

Area of Science:

• Microbiology
• Molecular Biology
• Pharmacology

Background:

• Bacterial resistance to aminoglycoside antibiotics is a significant clinical challenge.
• Mechanisms include target modification, altered drug transport, and enzymatic inactivation.
• Resistance can arise from chromosomal mutations or plasmid-mediated gene transfer.

Purpose of the Study:

• To investigate the prevalence and mechanisms of gentamicin resistance in Gram-negative bacteria.
• To identify specific aminoglycoside-modifying enzymes responsible for resistance.
• To determine the genetic basis (plasmid vs. chromosomal) of these resistance mechanisms.

Main Methods:

• Isolation and characterization of 475 Gram-negative bacterial strains from a university hospital.
• Phenotypic testing for gentamicin resistance.
• Enzymatic assays to detect aminoglycoside-modifying enzymes.
• Plasmid analysis to determine the genetic location of resistance genes.

Main Results:

• Approximately 10% of the 475 strains exhibited resistance to gentamicin.
• 44 out of 46 resistant strains produced aminoglycoside-modifying enzymes.
• Nucleotidyltransferase ANT-(2") was the most frequent enzyme, found in 88% of resistant Klebsiella strains.
• Acetylating enzymes AAC-(2"), AAC-(6"), and AAC-(3) were detected less frequently.
• All identified aminoglycoside transferases, except one AAC-(2"), were plasmid-encoded.

Conclusions:

• Aminoglycoside-modifying enzymes are the predominant mechanism of gentamicin resistance in the studied hospital isolates.
• Plasmid-mediated acquisition of resistance genes, particularly ANT-(2"), contributes significantly to multi-drug resistance.
• Understanding these mechanisms is crucial for developing strategies to combat antibiotic resistance.