Bacterial biocide resistance.

The emergence of bacterial resistance to antimicrobial agents has caused increasing concern globally. the basis of bacterial resistance to antibiotics is well known, while the nonsusceptibility mechanisms of bacteria to biocides are less well understood. Recently, there is considerable interest in the problems associated with the development and spread of bacterial nonsusceptibility to biocides in order to understand the mechanisms of action and the bacterial nonsusceptibility mechanisms to biocides. Different groups of bacteria vary in their intrinsic nonsusceptibility to biocides, with bacterial spores being the most resistant, followed by mycobacteria, then Gram-negative organisms, with Gram-positive bacteria generally being the most susceptible. this intrinsic nonsusceptibility in some instances might be associated with constitutive degradative enzymes or due to active efflux pumps, but in reality cellular impermeability is considered as a major factor that plays an important role in the emergence of bacterial nonsusceptibility to biocides. Nonsusceptibility associated with biofilmforming bacterial cells can be considered an intrinsic nonsusceptibility mechanism resulting from physiological (phenotypic) adaptation cells.

In vitro activity of cefepime and cefpirome compared to other third-generation cephem antibiotics against gram-negative nosocomial pathogens.

The in vitro activities of new expanded spectrum of fourth-generation cephalosporins, cefepime and cefpirome, were compared with those of three third-generation cephalosporins, cefoperazone, ceftazidime, and ceftriaxone, that are commonly used in the treatment of serious infections caused by aerobic gram-negative bacteria. The agar dilution method described by the US National Committee for Clinical Laboratory Standards was used to determine the minimum inhibitory concentrations of antibiotics tested. 302 clinical isolates, representing a cross-section of Klebsiella and Enterobacter species and Pseudomonas aeruginosa were tested. Cefepime was considerably more active than other antibiotics tested, against Klebsiella species and Enterobacter species, and demonstrated activity similar to ceftazidime against Pseudomonas aeruginosa. Ceftazidime was active against Pseudomonas aeruginosa but was less potent against Enterobacter species. Cefoperazone and ceftriaxone were less active than ceftazidime against Pseudomonas aeruginosa. Cefepime had slightly greater activity than cefpirome against the gram-negative bacteria tested. However, cefepime and cefpirome were found to be highly active against many resistant organisms that traditionally have been difficult to treat.

Comparative susceptibilities of Klebsiella species, Enterobacter species, and Pseudomonas aeruginosa to 11 antimicrobial agents in a tertiary-care university hospital.

The in vitro activity of cefepime was compared versus that of 10 antimicrobial agents commonly used in the treatment of serious infections caused by common aerobic gram-negative bacteria: aztreonam, cefoperazone, ceftazidime, ceftriaxone, ciprofloxacin, gentamicin, imipenem, piperacillin, ticarcillin-clavulanic acid, and tobramycin. We tested 30 clinical isolates representing a cross section of Klebsiella and Enterobacter species and Pseudomonas aeruginosa collected at our tertiary-care university hospital. The most potent beta-lactams were imipenem and cefepime, which demonstrated significant activity against the majority of strains in all 3 genera of bacteria tested, as did ciprofloxacin and tobramycin. Ceftazidime was active against Pseudomonas aeruginosa but was less potent against Klebsiella and Enterobacter spp. Cefoperazone and ceftriaxone were less active than ceftazidime against Pseudomonas aeruginosa. Cefepime was found to be highly active against many resistant organisms that traditionally have been difficult to treat.

A comparison of serial plate agar dilution, Bauer-Kirby disk diffusion, and the Vitek AutoMicrobic system for the determination of susceptibilities of Klebsiella spp., Enterobacter spp., and Pseudomonas aeruginosa to ten antimicrobial agents.

The use of rapid, automated technologies for assessment of antimicrobial susceptibility and determination of minimum inhibitory concentrations has been evolving for over a decade. We compared the Vitek AutoMicrobic system and Bauer-Kirby disk diffusion with the National Committee for Clinical Laboratory Standards methods of serial plate agar dilution for qualitative and quantitative susceptibilities of 301 hospital isolates of Klebsiella spp., Enterobacter spp., and Pseudomonas aeruginosa. Antibiotics tested were aztreonam, cefoperazone, ceftazidime, ceftriaxone, ciprofloxacin, gentamicin, imipenem, piperacillin, ticarcillin-clavulanic acid, and tobramycin. Agar dilution and Bauer-Kirby results were more strongly correlated for all three genera than were the results for agar dilution and Vitek. If agar dilution is presumed to be the "gold standard," Bauer-Kirby disk diffusion had only half the number of false susceptibles as did the Vitek. Thus, the Vitek AutoMicrobic system seems to be somewhat less reliable for both qualitative and quantitative measurement of susceptibility and resistance than is Bauer-Kirby disk diffusion.

Relationship of antibiotic resistance phenotype to the R-pyocin susceptibility pattern in clinical isolates of Pseudomonas aeruginosa.

One hundred sixteen clinical isolates of Pseudomonas aeruginosa were collected from 7 hospitals in Athens. All strains were studied for their susceptibility to cefotaxime, ceftazidime, carbenicillin, aztreonam, imipenem, nalidixic acid, ciprofloxacin, gentamicin, and chloramphenicol. In addition, the R-pyocin susceptibility pattern was determined and the strains were O-serotyped and tested for their agglutination in acriflavine. The isolates included 53 strains resistant to both gentamicin and carbenicillin, 13 to carbenicillin only, 20 to gentamicin only, and 30 sensitive to gentamicin and carbenicillin. The multiresistant isolates displayed relatively higher resistance to all other antibiotics except aztreonam and cefotaxime. Remarkably 30 out of 53 multiresistant isolates reacted with one pyocin only, namely pyocin R2. This R-pyocin response was not encountered in any other strains of the other antibiotic resistance phenotypes. These isolates belonged to the 0-12 serogroup. The 0-12 serogroup was represented only in a minority of strains giving other R-pyocin reactions. It is interesting that strains reacting with pyocin R5 only were mostly susceptible to antibiotics. The results clearly indicate lipopolysaccharide-core mutations in multiresistant clinical isolates of P. aeruginosa. Despite the fact that the R-pyocin resistance pattern can not define the precise possible defect, the multiple and high level resistance associated with R2-pyocin reaction seems to be an interesting trait.