Multicenter Study of the Clinical Efficacy of Imipenem/Cilastatin for Treatment of Serious Infections

Trumbore, David; Pontzer, Raymond; Levison, Matthew E.; Kaye, Donald; Cynamon, Michael H.; Liu, Chien; Hinthorn, Daniel R.; Tan, James S.; File, Thomas M.

doi:10.1093/clinids/7.supplement_3.s476

Cited by 20 publications

(7 citation statements)

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“…Several studies have suggested that P aeruginosa is the major nosocomial pathogen exhibiting imipenem resistance. 4,5,7,8 The finding that imipenem resistance among intensive care unit isolates is more frequent than among isolates from noncritical care units also has been reported. 8 Further, the respiratory tract has been the site of isolates with significant imipenem resistance in another report as well.…”

Section: Discussionmentioning

confidence: 94%

“…In recent years, several reports have emphasized the development of resistance to imipenem among gram-negative bacilli, especially Pseudomonas aeruginosa and Enterobacter species. [1][2][3][4][5][6][7][8] Emergence of resistance was observed, particularly in patients with the isolates were resistant to imipenem; 2.3% were either intermediate-susceptible or resistant to the drug. However, imipenem resistance for these isolates did not differ between the two periods and was not more common in patients in an intensive care unit or infections at any specific site.…”

Section: Introductionmentioning

confidence: 99%

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Resistance to Imipenem Among Selected Gram-Negative Bacilli in the United States

Gaynes

Culver

1992

Infect. Control Hosp. Epidemiol.

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The frequency of resistance to imipenem is greater among P aeruginosa than among Enterobacter species. Resistance to imipenem among the P aeruginosa isolates is more common from strains isolated from patients with nosocomial infections in an intensive care unit, from the respiratory tract, and from teaching hospitals. Resistance appears to be increasing among nosocomial P aeruginosa isolated in teaching hospitals.

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Section: Discussionmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Resistance to Imipenem Among Selected Gram-Negative Bacilli in the United States

Gaynes

Culver

1992

Infect. Control Hosp. Epidemiol.

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“…Although antecedent therapy with carbapenems, to which the bacterium is inherently resistant, has been cited by several authors as a risk factor (21,56,60,97,99,107,116,139,189,414,453), it is not a prerequisite for colonization or infection. Indeed, other investigators have highlighted many cases of S. maltophilia infection where patients had received broad-spectrum antibiotics other than imipenem, such as aminoglycosides, fluoroquinolones, and extended-spectrum cephalosporins (63,187,218,241).…”

Section: Epidemiologymentioning

confidence: 99%

Microbiological and Clinical Aspects of Infection Associated with Stenotrophomonas maltophilia

1998

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SUMMARY The gram-negative bacterium Stenotrophomonas maltophilia is increasingly recognized as an important cause of nosocomial infection. Infection occurs principally, but not exclusively, in debilitated and immunosuppressed individuals. Management of S. maltophilia-associated infection is problematic because many strains of the bacterium manifest resistance to multiple antibiotics. These difficulties are compounded by methodological problems in in vitro susceptibility testing for which there are, as yet, no formal guidelines. Despite its acknowledged importance as a nosocomial pathogen, little is known of the epidemiology of S. maltophilia, and although it is considered an environmental bacterium, its sources and reservoirs are often not readily apparent. Molecular typing systems may contribute to our knowledge of the epidemiology of S. maltophilia infection, thus allowing the development of strategies to interrupt the transmission of the bacterium in the hospital setting. Even less is known of pathogenic mechanisms and putative virulence factors involved in the natural history of S. maltophilia infection and this, coupled with difficulties in distinguishing colonization from true infection, has fostered the view that the bacterium is essentially nonpathogenic. This article aims to review the current taxonomic status of S. maltophilia, and it discusses the laboratory identification of the bacterium. The epidemiology of the organism is considered with particular reference to nosocomial outbreaks, several of which have been investigated by molecular typing techniques. Risk factors for acquisition of the bacterium are also reviewed, and the ever-expanding spectrum of clinical syndromes associated with S. maltophilia is surveyed. Antimicrobial resistance mechanisms, pitfalls in in vitro susceptibility testing, and therapy of S. maltophilia infections are also discussed.

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“…Analysis of the outer membrane proteins revealed a marked decrease of either a 46-or a 45-kilodalton protein. The lipopolysaccharide of the outer membrane in the imipenem-resistant variants was not altered.Within the last 2 years, several reports have emphasized the development of resistance to imipenem in clinical Pseudomonas aeruginosa isolates (1,8,10,19,22,24). Emergence of resistance was observed especially in patients suffering from either cystic fibrosis or nosocomial lower respiratory tract infections (1,19,22).…”

mentioning

confidence: 99%

Imipenem resistance in Pseudomonas aeruginosa resulting from diminished expression of an outer membrane protein

Büscher¹,

Cullmann²,

Dick³

et al. 1987

Antimicrob Agents Chemother

117

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The mechanism of Pseudomonas aeruginosa resistance to imipenem in five imipenem-susceptible clinical isolates and in their resistant counterparts was investigated. The frequency for selecting imipenem-resistant variants ranged from 2.7 x 10-5 to 2.1 x 10-8 and was comparable to those for other ,-lactams.Cross-resistance between imipenem and other 13-lactam compounds was not observed. In all imipenemresistant variants, induction of chromosomal j3-lactamase by imipenem was markedly diminished compared with that in the susceptible parent strain. This was not the case for other inducers such as ampicillin or cefoxitin, suggesting an impaired uptake of imipenem as an explanation for resistance. Analysis of the outer membrane proteins revealed a marked decrease of either a 46-or a 45-kilodalton protein. The lipopolysaccharide of the outer membrane in the imipenem-resistant variants was not altered.Within the last 2 years, several reports have emphasized the development of resistance to imipenem in clinical Pseudomonas aeruginosa isolates (1,8,10,19,22,24). Emergence of resistance was observed especially in patients suffering from either cystic fibrosis or nosocomial lower respiratory tract infections (1,19,22). Consequently, development of cross-resistance between imipenem and other ,B-lactam compounds must be evaluated.Enzymatic inactivation of imipenem has been reported thus far only for Pseudomonas maltophilia (21). Since resistance to newer cephalosporins and broad-spectrum penicillins is often chromosomally mediated, we studied five imipenem-susceptible clinical isolates of P. aeruginosa and their derived imipenem-resistant counterparts for the production of imipenem-inactivating enzymes and for outer membrane alterations. As it was not clear whether mutation or selection of a resistant subpopulation occurred, the term "variants" will be used for the resistant counterparts.MATERIALS AND METHODS Strains. The P. aeruginosa strains used were recent clinical isolates from our laboratory and were identified by standard procedures (12). Strain FRA was kindly supplied by G. Seibert, Frankfurt, Federal Republic of Germany. None of the strains exhibited resistance to antipseudomonal P-lactam compounds.MICs. MICs were determined in Mueller-Hinton broth (E. Merck AG, Darmstadt, Federal Republic of Germany) by twofold serial dilutions representing a final inoculum of 5 x 105 CFU/ml (microdilution procedure).Selection of resistant variants. Resistant variants were selected by plating 0.05 ml of an overnight culture in Trypticase soy broth (BBL Microbiology Systems, Cockeysville, Md.) onto Mueller-Hinton agar plates (Merck) containing the antibiotic in twofold serial dilution steps above the MIC. The frequency of resistant variants was expressed as the ratio of CFU grown in the presence of the antibiotic to the CFU of the control (grown without an antibiotic). All assays were carried out in triplicate. * Corresponding author.Kinetics of j3-lactamase production. ,B-Lactamase production was studied during exponential growth. Ove...

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Multicenter Study of the Clinical Efficacy of Imipenem/Cilastatin for Treatment of Serious Infections

Cited by 20 publications

References 7 publications

Resistance to Imipenem Among Selected Gram-Negative Bacilli in the United States

Resistance to Imipenem Among Selected Gram-Negative Bacilli in the United States

Microbiological and Clinical Aspects of Infection Associated with Stenotrophomonas maltophilia

Imipenem resistance in Pseudomonas aeruginosa resulting from diminished expression of an outer membrane protein

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