We conducted a case-series study of multiresistant Pseudomonas aeruginosa in patients who did not have cystic fibrosis. Patient characteristics, antibiotic exposures, time course of emergence of resistance, and clinical outcomes were examined. Twenty-two patients were identified from whom P. aeruginosa resistant to ciprofloxacin, imipenem, ceftazidime, and piperacillin was isolated. Nineteen (86%) had clinical infection. Patients received prolonged courses of antipseudomonal antibiotics before isolation of multiresistant P. aeruginosa. Nine of 11 patients with soft-tissue infection exhibited resolution of clinical infection but usually required surgical removal of infected tissue with or without revascularization. Overall, three patients died. In two instances in which multiple isolates with different susceptibility profiles from the same patient were available, pulsed-field gel electrophoresis profiles of serial isolates were indistinguishable or closely related. This study illustrates that multiresistant P. aeruginosa emerges in a stepwise manner after exposure to antipseudomonal antibiotics and results in adverse outcomes.
of 8.6 to 9.0 and one with a pI value of approximately 9.5. The enzyme with the higher pI in each strain hydrolyzed carbapenems and was not inhibited by EDTA, similar to the chromosomal class A SME-1 -lactamase isolated from the 1982 London strain S. marcescens S6. The genes encoding the carbapenem-hydrolyzing enzymes were cloned in Escherichia coli and sequenced. The enzyme from the Minnesota isolate had an amino acid sequence identical to that of SME-1. The isolates from Boston and UCLA produced SME-2, an enzyme with a single amino acid change relative to SME-1, a substitution from valine to glutamine at position 207. Purified SME enzymes from the U.S. isolates had -lactam hydrolysis profiles similar to that of the London SME-1 enzyme. Pulsed-field gel electrophoresis analysis revealed that the isolates showed some similarity but differed by at least three genetic events. In conclusion, a family of rare class A carbapenem-hydrolyzing -lactamases first described in London has now been identified in S. marcescens isolates across the United States.
In vitro, the antimicrobial agent taurolidine inhibited virtually all of the bacteria tested, including vancomycin-resistant enterococci, oxacillin-resistant staphylococci, and Stenotrophomonas maltophilia, at concentrations between 250 and 2,000 g/ml. Taurolidine was not effective in experimental endocarditis. While it appears unlikely that this antimicrobial would be useful for systemic therapy, its bactericidal activity and the resistance rates found (<10 ؊9 ) are favorable indicators for its possible development for topical use.With the continuing emergence of multiply antibiotic-resistant organisms, the need to develop new therapeutic agents remains evident. Taurolidine [bis-(1,1-dioxoperhydro-1,2,4-thiadiazinyl-4)methane], a derivative of the amino acid taurine, is an antimicrobial agent which inhibits and kills a broad range of microorganisms in vitro, albeit at high concentrations (3,4,9,11,13). This compound acts through mechanisms unlike those described for other currently available antimicrobials. Specifically, it is believed that methylol derivatives interact with components of bacterial cell walls resulting in irreparable injury (4). Taurolidine also appears to have immunoregulatory properties, blunting lipopolysaccharide-induced tumor necrosis factor and interleukin-1 release from human peripheral blood mononuclear cells (2) and also reducing adherence of bacteria to human epithelial cells in vitro (5). The compound has been given to humans both intravenously (i.v.) and by peritoneal lavage (1, 12).The purpose of the present study was to examine the in vitro activity of taurolidine against a broad variety of bacterial species, including antibiotic-resistant strains. We also evaluated the activity of taurolidine in vivo in experimental endocarditis using two strains of enterococci, one of which was a vancomycin-resistant strain of Enterococcus faecium.Most of the bacterial strains used in this study were routine isolates collected by our clinical microbiology laboratory during 1997. Additional strains from our collection were included based upon specific resistance traits. Taurolidine was provided by Wallace Laboratories, Cranbury, N.J. Antimicrobial reference standards of ciprofloxacin, imipenem, and cefotaxime were provided by Bayer Corporation, West Haven, Conn.; Merck & Co., Inc., West Point, Pa.; and Hoechst Marion Roussel, Inc., Kansas City, Mo., respectively. Vancomycin was obtained from Eli Lilly & Co., Indianapolis, Ind. MICs were determined by agar dilution (7, 8) on Mueller-Hinton II agar (BBL Microbiology Systems, Cockeysville, Md.) except as noted otherwise. Agar was supplemented with 5% sheep blood for streptococci and diphtheroids. Inocula were ca. 10 4 (10 5 for anaerobes) CFU/spot. Plates were incubated in room air and read at 18 to 20 h, except for lactobacilli, Leuconostoc spp., Pediococcus spp., and pneumococci, which were incubated in 5% CO 2 and examined for growth at 24 h. Anaerobes were incubated for 48 h on brucella agar in an atmosphere produced by Gas-Pak Plus (BBL). Time-...
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