Mechanisms of resistance to five aminoglycoside antibiotics: gentamicin (G), tobramycin (T), netilmicin (N), amikacin (A) and isepamicin (I), were assessed in 16 clinical isolates of Pseudomonas aeruginosa serotype O11, originating from five hospitals in Bratislava. All isolates were in vitro highly resistant to all mentioned aminoglycoside antibiotics (MIC > 32 mg/l). Thirteen isolates produced three aminoglycoside-modifying enzymes (AGME), responsible for resistance to the respective aminoglycosides: AAC(6')-I (T, N, A); APH (2") (G, T); APH (3')-VI (I). In addition to this, in four isolates a production of AAC(3)-II (G, T, N) was observed. In three isolates no production of AGME was observed. The strains studied were isolated mainly from urine. Several isolates were able to transfer aminoglycoside resistance by bacterial conjugation to P. aeruginosa 1008 rifr recipient. The transconjugants from these transfers expressed the same resistance pattern and nearly the same mechanisms of resistance as the donor strains.