Pseudomonas aeruginosa in community-acquired urinary tract infection: AFORCOPIBIO 1995-1996

32 P. aeruginosa strains were collected by ten private clinical laboratories in patients with community-acquired urinary tract infections during a prospective multicenter study performed during two 2-month periods (May and June) in 1995 and 1996. All non hospitalised patients in the past 3 months were included. Minimal inhibitory concentrations were determined by Mueller Hinton agar dilution for ticarcillin, piperacillin, ceftazidime, imipenem, ciprofloxacin, amikacin, and fosfomycin. Mechanisms of resistance were determined for all beta-lactam resistant strains by iso-electric focusing, and when a strain did not produce penicillinase, the specific beta-lactamase activity was quantified. P. aeruginosa was unfrequently isolated (1.5 %). The highest rates of susceptibility were shown for ceftazidime and imipenem (respectively 96.9 % and 90.6 %). Susceptibility was lower for ticarcillin (50 %), piperacillin (84.3 %), fluoroquinolones (56.2 %), amikacin (62.5 %), and fosfomycin (62.5 %). Two resistance mechanisms to beta-lactams were involved in P. aeruginosa: non enzymatic resistance (9 strains) and production of penicillinase PSE-1 (7 strains).