Abstract
The mechanisms of resistance to aminoglycoside antibiotics in Gram-negative nosocomial pathogens isolated in four Russian hospitals were studied. The most common and almost exclusive mechanism of aminoglycoside resistance was production of aminoglycoside-modifying enzymes. Various phenotypes of resistance were found. In Smolensk Regional Hospital the most common phenotype of resistance was gentamicin-tobramycin (54,4%, due to ANT(2”) enzyme) and gentamicin-tobramycin-netilmycin (36,1% – AAC(3)-V or combination of ANT(2”)+AAC(3)-Ia enzymes). The same phenotypes were predominant in Krasnodar Regional Hospital. In Central Clinical Hospital (Moscow) in addition to gentamicin-tobramycin (29,2%) and gentamicin-tobramycin-netilmycin (36,6%) phenotypes the cross-resistance to 2nd and 3rd aminoglycoside generations has been found: gentamicin-amikacin-isepamycin phenotype of resistance [due to combination of APH(3’)-VI+AAC(3)-I enzymes] – in 4,9% of strains, gentamicin-tobramycin-amikacin-isepamycin phenotype [due to combination of APH(3’)-VI+ANT(2”)] – in 9,8%, gentamicin-tobramycin-netilmycin-amikacin phenotype [due to combination of AAC(6’)-I+ANT(2”) enzymes] – in 4,9%. In Main Military Clinical Hospital (Moscow) the following resistance phenotypes were detected: gentamicin-tobramycin [production of ANT(2”) enzyme] – 20,4%, gentamicin-tobramycin-netilmycin [AAC(3)-V or combination of ANT(2”)+AAC(6’)-I enzymes] – 24,1%, gentamicin-tobramycin-netilmycin-amikacin-isepamycin [due to combination of APH(3’)-VI+AAC(3)-V or APH(3’)-VI+ANT(2”)+AAC(6’)-I enzymes] – 12,9%, gentamicin-tobramycin-amikacin-isepamycin [due to combination of APH(3’)-VI+ANT(2”) enzymes] – 25,9%, amikacin-isepamycin [APH(3’)-VI enzyme] – 11,1%.
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