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[Comparative study of apramycin-resistant microorganisms isolated from man and animals]
Abstract:
Apramycin-modifying strains isolated from pigs with coli bacteriosis, from humans and hospital environment were studied comparatively. Production of enzymes modifying the aminoglycoside was estimated with the radioactive cofactor procedure. E. coli isolates from the animals were phenotypically resistant to apramycin and a number of other aminoglycosides. They produced acetyltransferase AAC(3)IV, phosphotransferase APH(3')(5"), APH(3") and other enzymes. Resistance of the strains to gentamicin was also conditioned by AAC(3)IV since these strains did not produce AAD(2") and AAC(6'). In the resistant strains of E. coli and their transconjugates there were detected plasmids with a relative molecular weight of 60-80 MD. Some of the belonged to the compatibility group I1, the others belonged to the compatibility group H1. Strains of S. marcescens, K. pneumoniae. K. oxytoca and S. aureus isolated from humans and hospital environment were sensitive to apramycin. Only isolates of P. aeruginosa were resistant to this antibiotic. However, all the isolates produced AAC(3)IV. Some of them additionally produced AAC(6'), an enzyme modifying amikacin, kanamycin and other antibiotics and not acetylating apramycin. Almost all the strains produced kanamycin- and streptomycin phosphotransferases. Possible coselection of strains resistant to apramycin and gentamicin using one of these aminoglycosides is discussed.
Insights
Apramycin resistance in E. coli from pigs is linked to specific aminoglycoside-modifying enzymes like AAC(3)IV, often located on plasmids. Other bacteria showed varied resistance, with P. aeruginosa producing AAC(3)IV and other enzymes.
Area of Science:
- Microbiology
- Molecular Biology
- Antimicrobial Resistance
Background:
- Aminoglycoside antibiotics, including apramycin, are crucial in treating bacterial infections.
- The emergence of antibiotic resistance, particularly in Gram-negative bacteria like E. coli, poses a significant public health threat.
- Understanding the mechanisms of resistance is vital for developing effective treatment strategies.
Purpose of the Study:
- To comparatively study apramycin-modifying bacterial strains isolated from various sources (pigs, humans, hospitals).
- To identify the specific enzymes responsible for apramycin modification and their genetic basis.
- To investigate the potential for coselection of resistance to apramycin and other aminoglycosides like gentamicin.
Main Methods:
- Isolation and characterization of bacterial strains from pigs, humans, and hospital environments.
- Enzymatic assays using radioactive cofactors to quantify aminoglycoside-modifying enzyme production.
- Phenotypic resistance profiling against apramycin and other aminoglycosides.
- Plasmid analysis, including molecular weight determination and compatibility grouping.
- Conjugation experiments to transfer resistance traits.
Main Results:
- E. coli isolates from pigs exhibited resistance to apramycin and other aminoglycosides, producing acetyltransferase AAC(3)IV and phosphotransferases APH(3")(5") and APH(3").
- Gentamicin resistance in these E. coli strains was also mediated by AAC(3)IV.
- Resistant E. coli strains harbored plasmids (60-80 MD) belonging to compatibility groups I1 and H1.
- While most other tested bacteria (S. marcescens, K. pneumoniae, K. oxytoca, S. aureus) were sensitive to apramycin, P. aeruginosa isolates were resistant, all producing AAC(3)IV.
- Some P. aeruginosa strains also produced AAC(6"), which modifies other aminoglycosides but not apramycin, and most strains produced kanamycin- and streptomycin phosphotransferases.
Conclusions:
- Apramycin resistance in E. coli is primarily mediated by AAC(3)IV, often plasmid-located.
- The presence of AAC(3)IV in resistant P. aeruginosa suggests a broader role for this enzyme in aminoglycoside resistance.
- The study highlights the potential for coselection of resistance to apramycin and gentamicin, emphasizing the need for careful antibiotic stewardship.