Bacterial resistance to aminoglycoside antibiotics can occur by a variety of mechanisms (including alteration of the drug target site, interference with drug transport into the cell, or enzymatic detoxification of the antibiotics) due to chromosomal mutations or the inheritance of new genetic information mediated by resistance plasmids. Studies with 475 gram-negative bacteria isolated at the university hospital Bonn revealed that about 10% of the strains were resistant to gentamicin. 44 of 46 strains produced aminoglycoside modifying enzymes; the remaining two strains do not produce detectable enzymatic activity. Among those aminoglycoside transferases causing multiresistance to modern aminoglycosides, the nucleotidyltransferase ANT-(2") occurs most frequently and accounts for 88% of the gentamicin resistant klebsiella strains. The gentamicin acetylating enzymes AAC-(2'), AAC-(6'), and AAC-(3) are detected less frequently. All aminoglycoside transferases, except one acetyltransferase AAC-(2') from Proteus vulgaris, were found to be plasmid encoded.