M. Kettner et al., INCIDENCE AND MECHANISMS OF AMINOGLYCOSIDE RESISTANCE IN PSEUDOMONAS-AERUGINOSA SEROTYPE-O11 ISOLATES, Infection, 23(6), 1995, pp. 380-383
Mechanisms of resistance to five aminoglycoside antibiotics: gentamici
n (G), tobramycin (T), netilmicin (N), amikacin (A) and isepamicin (I)
, were assessed in 16 clinical isolates of Pseudomonas aeruginosa sero
type 011, originating from five hospitals in Bratislava. All isolates
were in vitro highly resistant to all mentioned aminoglycoside antibio
tics (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'))-V
I (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 ob
served. The strains studied were isolated mainly from urine. Several i
solates were able to transfer aminoglycoside resistance by bacterial c
onjugation to P. aeruginosa 1008 rip(r) recipient. The transconjugants
from these transfers expressed the same resistance pattern and nearly
the same mechanisms of resistance as the donor strains.