1984•American Journal of Clinical PathologyRequires access

Aminoglycoside Resistance in Pseudomonas aeruginosa Isolated from Cystic Fibrosis Patients

William F. McNeill, Joseph F. John, James A. Twitty

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Abstract

The authors studied 30 gentamicin-resistant and 17 gentamicin-sensitive strains of Pseudomonas aeruginosa isolated from respiratory cultures of patients with cystic fibrosis from five United States cities for the presence of plasmids, cross-resistance to other aminoglycosides, and the production of aminoglycoside-modifying enzymes. Four of 30 resistant strains and 3 of 17 sensitive strains contained one or more plasmids. Aminoglycoside cross-resistance to tobramycin, amikacin, and netilmicin was seen in 21 of 30 gentamicin-resistant strains. Seven strains that had low-level gentamicin resistance (minimum inhibitory concentrations [MIC] = 8-32 micrograms/mL) were sensitive to one or more of the other three aminoglycosides. Two strains with high-level gentamicin resistance (MIC greater than or equal to 128 micrograms/mL) were sensitive to amikacin. These two strains, each containing three plasmids, were the only isolates of nine tested that produced an aminoglycoside-modifying enzyme with activity against gentamicin. None of the plasmids was transferable by conjugation. Four strains, three of which contained one or more plasmids, produced an aminoglycoside 3'-0-phosphotransferase II. The authors propose that the mechanism of gentamicin resistance in P. aeruginosa from patients with cystic fibrosis is not commonly plasmid-mediated and likely is due to membrane impermeability to aminoglycosides.

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What this paper is about

The authors studied 30 gentamicin-resistant and 17 gentamicin-sensitive strains of Pseudomonas aeruginosa isolated from respiratory cultures of patients with cystic fibrosis from five United States cities for the presence of plasmids, cross-resistance to other aminoglycosides, and the production of aminoglycoside-modifying enzymes. Four of 30 resistant strains and 3 of 17 sensitive strains contained one or more plasmids. Aminoglycoside cross-resistance to tobramycin, amikacin, and netilmicin was seen in 21 of 30 gentamicin-resistant strains. Seven strains that had low-level gentamicin resistance (minimum inhibitory concentrations [MIC] = 8-32 micrograms/mL) were sensitive to one or more of the other three aminoglycosides. Two strains with high-level gentamicin resistance (MIC greater than or equal to 128 micrograms/mL) were sensitive to amikacin. These two strains, each containing three plasmids, were the only isolates of nine tested that produced an aminoglycoside-modifying enzyme with activity against gentamicin. None of the plasmids was transferable by conjugation. Four strains, three of which contained one or more plasmids, produced an aminoglycoside 3'-0-phosphotransferase II. The authors propose that the mechanism of gentamicin resistance in P. aeruginosa from patients with cystic fibrosis is not commonly plasmid-mediated and likely is due to membrane impermeability to aminoglycosides.

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Available abstract

The authors studied 30 gentamicin-resistant and 17 gentamicin-sensitive strains of Pseudomonas aeruginosa isolated from respiratory cultures of patients with cystic fibrosis from five United States cities for the presence of plasmids, cross-resistance to other aminoglycosides, and the production of aminoglycoside-modifying enzymes. Four of 30 resistant strains and 3 of 17 sensitive strains contained one or more plasmids. Aminoglycoside cross-resistance to tobramycin, amikacin, and netilmicin was seen in 21 of 30 gentamicin-resistant strains. Seven strains that had low-level gentamicin resistance (minimum inhibitory concentrations [MIC] = 8-32 micrograms/mL) were sensitive to one or more of the other three aminoglycosides. Two strains with high-level gentamicin resistance (MIC greater than or equal to 128 micrograms/mL) were sensitive to amikacin. These two strains, each containing three plasmids, were the only isolates of nine tested that produced an aminoglycoside-modifying enzyme with activity against gentamicin. None of the plasmids was transferable by conjugation. Four strains, three of which contained one or more plasmids, produced an aminoglycoside 3'-0-phosphotransferase II. The authors propose that the mechanism of gentamicin resistance in P. aeruginosa from patients with cystic fibrosis is not commonly plasmid-mediated and likely is due to membrane impermeability to aminoglycosides.

Key concepts: Aminoglycoside, Amikacin, Tobramycin, Netilmicin, Gentamicin, Microbiology, Plasmid, Pseudomonas aeruginosa

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