The aim of this study was to establish the clinical features of extraintestinal infections caused by Hafnia alvei. Over a 5-year period (1994-1998), data were collected regarding inpatients (n = 8) with nosocomial (n = 5) or community-acquired (n = 3) infections caused by Hafnia alvei. The mean age of the patients was 47 +/- 21 years. Three patients had hospital-acquired urinary tract infections. Hafnia alvei also caused community-acquired cholangitis, cholecystitis, appendicitis, psoas abscess and prosthetic endocarditis. Hafnia alvei was susceptible to amoxicillin/clavulanic acid and to first-generation cephalosporins in two cases. Susceptibility to aminoglycosides, imipenem, cotrimoxazole, ciprofloxacin, piperacillin and cefotaxime was very good (8/8). Four patients required invasive treatment.

No abstract

Four strains of Pseudomonas aeruginosa obtained from clinical isolates which are carbenicillin resistant were studied to find the cause(s) of resistance to this beta-lactam antibiotic. The electrophoresis patterns of the four strains (PH20610, PH20815, PH4011, and PH4301) were found to be different from those of a wild-type strain, P. aeruginosa NCTC 10662, and appeared to lack penicillin-binding protein 2. Affinity of other penicillin-binding proteins from strains PH20610 and PH20815 for carbenicillin seemed to be normal or slightly diminished. Electrophoretic patterns of penicillin-binding proteins from strains PH4011 and PH4301 had more profound differences, since the affinities of their penicillin-binding proteins 1a, 1b, and 4 for carbenicillin were decreased by nearly two orders of magnitude relative to the preparations from the wild-type strain. Kinetic studies on binding of carbenicillin to penicillin-binding proteins both in isolated membrane preparations and in intact cells revealed that carbenicillin penetration into resistant cells was a much slower process than in susceptible cells, suggesting that the outer envelope structures serve as an efficient barrier against carbenicillin entry into our P. aeruginosa strains from clinical isolates.

No abstract

No abstract