Disease relevance of Enterobacter

• Cephalosporin hyper-resistant Enterobacter cloacae strains are isolated with increasing frequency from hospital infections [1].
• Clinical experience shows that trimethoprim-sulfamethoxazole may be beneficial in the treatment of gram-negative bacillary meningitis caused by organisms only moderately susceptible to third-generation cephalosporins (Enterobacter cloacae, Serratia marcescens) or resistant to these antibiotic agents (Pseudomonas cepacia, Acinetobacter) [2].
• Pyridoxal phosphate-dependent histidine decarboxylases. Cloning, sequencing, and expression of genes from Klebsiella planticola and Enterobacter aerogenes and properties of the overexpressed enzymes [3].
• The research program thus initiated has shown that bacteria such as Enterobacter cloacae can grow in up to 25% SDS and that SDS-shock proteins constitute c. 8% of the proteins synthesized by SDS-grown Escherichia coli [4].
• These compounds were also found in cell-free supernatants from Proteus mirabilis, Citrobacter freundii and Enterobacter agglomerans [cyclo(DeltaAla-L-Val) only] [5].

High impact information on Enterobacter

• A phosphonate monoester, m-carboxyphenyl phenylacetamidomethylphosphonate, has been found to be a specific inhibitor of the class C beta-lactamase of Enterobacter cloacae P99 [6].
• Enterobacter resistant to amoxycillin/clavulanate [7].
• Analysis of a carbapenem-hydrolyzing class A beta-lactamase from Enterobacter cloacae and of its LysR-type regulatory protein [8].
• Cephalosporin doxorubicin (C-Dox) and 7-(4-carboxybutanamido)-cephalosporin mustard (CCM) are prodrugs that are catalytically converted by Enterobacter cloacae beta-lactamase (bL) to the active anticancer agents doxorubicin and phenylenediamine mustard, respectively [9].
• Atomic resolution structures and solution behavior of enzyme-substrate complexes of Enterobacter cloacae PB2 pentaerythritol tetranitrate reductase. Multiple conformational states and implications for the mechanism of nitroaromatic explosive degradation [10].

Chemical compound and disease context of Enterobacter

• Purification and characterization of indolepyruvate decarboxylase. A novel enzyme for indole-3-acetic acid biosynthesis in Enterobacter cloacae [11].
• Purification and characterization of PrbA, a new esterase from Enterobacter cloacae hydrolyzing the esters of 4-hydroxybenzoic acid (parabens) [12].
• Purification and characterization of an oxygen-insensitive NAD(P)H nitroreductase from Enterobacter cloacae [13].
• The presence of a previously unidentified enzyme, tentatively designated 5-methylthioribose kinase, has been demonstrated in cell-free extracts of Enterobacter aerogenes [14].
• The crystal structure of the nitroreductase enzyme from Enterobacter cloacae has been determined for the oxidized form in separate complexes with benzoate and acetate inhibitors and for the two-electron reduced form [15].

Biological context of Enterobacter

• Here we demonstrate the feasibility of this approach by using a well-studied enzyme-catalyzed reaction, cephalosporin hydrolysis by the Enterobacter cloacae P99 cephalosporinase (beta-lactam hydrolase, EC ) [16].
• BLIP-I inhibited Bacto(R) Penase (Difco), and plasmid encoded TEM-1 beta-lactamase, whereas it did not inhibit Enterobacter cloacae beta-lactamases [17].
• Unlike the well-studied class C ES beta-lactamase from Enterobacter cloacae GC1, the Omega-loop does not affect the active site conformation and the catalytic activity of CMY-10 [18].
• Among these, 6 other Enterobacteriaceae, Salmonella, Shigella, Klebsiella, Citrobacter, Hafnia, and Enterobacter species, contained DNA sequences that hybridized to the probe under high-stringency conditions [19].
• mar Operon involved in multidrug resistance of Enterobacter aerogenes [20].

Anatomical context of Enterobacter

• The resistance of certain gram-negative bacilli to temocillin seemed to be a result of failure of the molecule to enter through the cell wall, since combination of temocillin with EDTA made Pseudomonas, Acinetobacter, and Enterobacter strains susceptible to low concentrations of the compound [21].
• Serum C reactive protein (CRP) and erythrocyte sedimentation rate (ESR) were measured on 469 occasions in 149 patients with ankylosing spondylitis who had also been investigated for faecal carriage of klebsiella/enterobacter species on the same occasions [22].
• The high prevalence of opportunistic colonizing organisms persisted at follow-up (48%) with a significant excess of new organisms (Enterobacter cloacae, Klebsiella species and Candida species) present in sputum in the amoxycillin-treated patients [23].
• Immobilized cells of Enterobacter agglomerans, able to reduce azo dyes enzymatically, were used as a biocatalyst for the decolorization of synthetic medium containing the toxic azo dye methyl red (MR) [24].
• The chemotactic activity of chicken blood mononuclear leukocytes was examined in partially-developed 15I5-B-congenic chicken lines using Enterobacter cloacae culture supernatant and formyl-methionyl-leucyl-phenylanine (f-met-leu-phe) (10(-5)M) [25].

Gene context of Enterobacter

• In clinical isolates of Enterobacter cloacae, resistance to the newer beta-lactam antibiotics often results from overproduction of a cephalosporinase encoded by the beta-lactam-inducible ampC gene [26].
• ampG is essential for high-level expression of AmpC beta-lactamase in Enterobacter cloacae [27].
• A recombinant fusion protein, L49-sFv-bL, that contains the antibody binding regions of L49 fused to the Enterobacter cloacae r2-1 beta-lactamase (bL) was constructed, expressed, and purified to homogeneity in an Escherichia coli soluble expression system [28].
• To study the function of the OmpX protein and its role in the regulation of porin protein synthesis, the ompX gene was deleted from the Enterobacter cloacae chromosome and replaced by the aphA gene [29].
• Detection of mutations in the gyrA and parC genes in quinolone-resistant clinical isolates of Enterobacter cloacae [30].

Analytical, diagnostic and therapeutic context of Enterobacter

• Minimum inhibitory concentrations (MICs) of cefmenoxime were determined and all pathogens were inhibited by 12.5 micrograms/ml or less, except for Enterobacter cloacae and Acinetobacter species, both of which had an MIC of 25.0 micrograms/ml [31].
• Two hundred eighty-two cases with a third-generation cephalosporin-resistant pathogen (203 with Enterobacter spp., 50 with Pseudomonas aeruginosa, and 29 with Klebsiella pneumoniae) were matched on length of stay to controls in a 1:2 ratio [32].
• A cysteine residue has been substituted for the active-site serine of the class-C beta-lactamase produced by Enterobacter cloacae 908R by site-directed mutagenesis [33].
• Molecular typing was used to investigate an outbreak of infection caused by multidrug-resistant Enterobacter aerogenes (MREA) susceptible only to gentamicin and imipenem in an intensive care unit (ICU) [34].
• The UDP-N-acetylglucosamine 1-carboxyvinyl-transferase of Enterobacter cloacae. Molecular cloning, sequencing of the gene and overexpression of the enzyme [35].

References