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PubMed1998

Immuno-detection of the virulence determinant OmpX at the cell surface of Enterobacter cloacae.

A model for the topology of the Enterobacter cloacae outer membrane protein OmpX has been proposed, based on the primary sequence and on analogy to homologous proteins. According to this model the membrane embedded part of the protein consists of eight antiparallel beta-strands. Four random coil loops are located at the bacterial surface and three beta-turns at the periplasmic side of the membrane. Antibodies were raised against synthetic peptides representing five OmpX domains, four of which are putative peripheral and one located in the membrane. The accessibilities of OmpX to these antibodies were tested in intact cells by immuno-gold electron microscopy. This study showed that OmpX is indeed an outer membrane protein, the N-proximal loop of which forms an IgG-accessible epitope at the cell surface.

Amino Acid Sequence↗
PubMed1999

Glycosylation of the Enterobacter cloacae outer membrane protein OmpX in eukaryotic cells.

The topological model of the Enterobacter cloacae outer membrane protein OmpX showed three putative glycosylation sites. When OmpX was expressed in bacteria that were cultured under aerated conditions, no glycosylation was observed. The coupling of carbohydrate chains to the ompX gene product was also investigated in the eukaryotic baculovirus expression system. For this purpose, a recombinant ompX gene-containing baculovirus was made. Infection of insect cells with this recombinant virus resulted in the production of sufficient amounts of OmpX to study glycosylation. In this system, all potential N-glycosylation sites of OmpX were utilized. Furthermore, it became clear that glycosylated OmpX was retained in the insect cells and was not secreted in the medium. Given the fact that OmpX plays a role in the invasion of E. cloacae in rabbit enterocytes, glycosylation of this protein occurring only under specific conditions may be involved in this process.

Amino Acid Sequence↗
PubMed2001

Extension of resistance to cefepime and cefpirome associated to a six amino acid deletion in the H-10 helix of the cephalosporinase of an Enterobacter cloacae clinical isolate.

Enterobacter cloacae CHE, a clinical strain with overproduced cephalosporinase was found to be highly resistant to the new cephalosporins, cefepime and cefpirome (MICs> or =128 microg ml(-1)). The strain was isolated from a child previously treated with cefepime. The catalytic efficiency of the purified enzyme with the third-generation cephalosporins, cefepime and cefpirome, was 10 times higher than that with the E. cloacae P99 enzyme. This was mostly due to a decrease in K(m) for these beta-lactams. The clinical isolate produced large amounts of the cephalosporinase because introduction of the ampD gene decreased ampC expression and partially restored the wild-type phenotype. Indeed, MICs of cefepime and cefpirome remained 10 times higher than those for a stable derepressed clinical isolate (OUDhyp) transformed with an ampD gene. Sequencing of the ampC gene showed that 18 nucleotides had been deleted, corresponding to the six amino acids SKVALA (residues 289--294). According to the crystal structure of P99 beta-lactamase, this deletion was located in the H-10 helix. The ampR-ampC genes from the clinical isolates CHE and OUDhyp were cloned and expressed in Escherichia coli JM101. The MICs of cefpirome and cefepime of E. coli harboring ampC and ampR genes from CHE were 100--200 times higher than those of E. coli harboring ampC and ampR genes from OUDhyp. This suggests that the deletion, confirmed by sequencing of the ampC gene, is involved in resistance to cefepime and cefpirome. However, the high level of resistance to cefepime and cefpirome observed in the E. cloacae clinical isolate was due to a combination of hyperproduction of the AmpC beta-lactamase and structural modification of the enzyme. This is the first example of an AmpC variant conferring resistance to cefepime and cefpirome, isolated as a clinical strain.

Amino Acid Sequence↗
PubMed2006

Enterobacter sp. VKGH12 growing with n-butanol as the sole carbon source and cells to which the alcohol is added as pure toxin show considerable differences in their adaptive responses.

The solvent-tolerant bacterium Enterobacter sp. VKGH12 is able to grow in toxic concentrations of n-butanol up to 1.5 % (volume in volume) as the sole carbon and energy source. Morphology changes in the cells growing on increasing concentrations of n-butanol were observed. The size of the bacteria decreased with increasing concentrations of n-butanol, also leading to an enhanced ratio between the surface and volume of the cells. This is in complete contradiction to the reaction of glucose-grown cells to which n-butanol had been added as a toxin. Similar differences were found in typical adaptive responses to toxic organic compounds, namely changes in fatty acid composition of membrane lipids and the activity of catalase. In both cases, reactions depending on the n-butanol concentrations could be observed when the toxin was added to glucose-grown cells, whereas no reaction was observable when the cells were growing in n-butanol as the sole carbon and energy source. This is another proof for the observation that there are certain differences between the adaptive strategies of cells when adapting to high concentrations of a growth substrate and those when adapting to a toxin added to growing cells.

1-Butanol↗
PubMed1994

Enterobacter cloacae causing pneumatocele in a neonate.

Pneumatocele formation, a cyst-like rarefaction that develops within the lung parenchyma, is an unusual complication of pneumonia in the neonate. It has been reported to occur with Staphlococcus aureus, Escherichia coli, Klebsiella pneumoniae, Streptococcus pneumoniae, and Pseudomonas aeruginosa infections. We describe a case of a premature neonate with pneumonia and subsequent pneumatocele formation caused by Enterobacter cloacae.

Cysts↗
PubMed1986

Clinical strains of Enterobacter agglomerans (synonyms: Erwinia herbicola, Erwinia milletiae) identified by DNA-DNA-hybridization.

Using DNA-DNA-hybridization it could be shown that 52 of 86 clinical isolates of Enterobacter agglomerans were closely related to each other, to the type strain of the species and also to the type strains of Erwinia herbicola and Erwinia milletiae. Most of the strains investigated were of the biogroups 1 and G1 of Ewing & Fife. All strains of the genetically defined group belonged to these two biogroups; none of these isolates fermented dulcitol, and with few exceptions they were also cellobiose, lactose and sorbitol negative.

DNA, Bacterial↗
PubMed1987

Comparison of resistance types in Enterobacter cloacae 1977 and 1985.

A collection of Enterobacter cloacae strains from Odense University Hospital from 1977 were compared with a collection from 1985 as regards acquired resistance traits. Among the strains with carbenicillin (Ca) resistance, the number of multiresistant strains decreased while the number with sole Ca-resistance increased. In 1977, a high proportion of the Ca-resistant (Ca-r) strains had plasmid-mediated beta-lactam resistance, but in 1985 the Ca-r strains were completely dominated by organisms with elevated amounts of chromosomally-mediated beta-lactamase. The latter, but not the former, strains were resistant to the newer cephalosporins (e.g. cefotaxime (Ctax)). The consumption of Ctax and cefuroxime increased from 0 kg in 1977 to 7.0 kg in 1985. It is therefore probable that this increase was the cause of the change in occurrence of the resistance types. Ninety-one % of the Ca-r strains were isolated from urinary samples in 1977. The percentage was only 31 in 1985. This change, concomitant with the increase in Ctax-r strains, can probably be explained by the better conditions for selection of Ctax-r mutants, producing greater amounts of chromosomal beta-lactamase, in wounds and respiratory tract than in urine.

Ampicillin Resistance↗
PubMed1991

Phenotypical properties of Enterobacter agglomerans (Pantoea agglomerans) from human, animal and plant sources.

Clinical, animal and plant isolates, representing different geographical areas, were identified as Enterobacter agglomerans (Pantoea agglomerans) using a quantitative bacterial dot method for DNA-DNA hybridization. The phenotypical properties of the 65 strains were investigated by conventional test methods. No strain decarboxylated ornithine. Twenty-two strains, mainly plant isolates, showed delayed acid production from alpha-methyl-glycoside, a trait which may have ecological significance. With regard to these two properties, our results differed from the description of Pantoea agglomerans given by Gavini et al. (6); further investigations will clarify these differences. Three non-pigmented, maltose-negative and salicin-negative variants were derived from yellow pigmented, maltose-positive, salicin-positive strains.

Animals↗
PubMed1993

Biotyping, phage typing, and O-serotyping of clinical isolates of Enterobacter cloacae.

The purpose of this study was to make an independent evaluation of the methods of bio-, phage-, and O-serotyping which had been used only in the laboratory of origin, and to assess the extent of possible cross-infection of Enterobacter cloacae in a Danish university hospital. The material consisted of 237 clinical isolates of E. cloacae from the clinical microbiology laboratory at Hvidovre Hospital. The typability of bio-, phage-, and serotyping was 100%, 83%, and 85%, respectively. Reproducibility of serotyping was 90% and of phage typing 96% if two major differences were allowed to differentiate between patterns. O-serotyping had the highest discriminatory power and combination of all typing methods further increased discrimination. Outbreaks of E. cloacae were not evident in clinical departments, but cross-infections from one department to another could not be completely ruled out. We concluded that the combination of bio-, phage- and O-serotyping is sufficiently discriminating and will be satisfactory in the majority of clinical situations.

Bacteriophage Typing↗
PubMed1993

Ribotyping of selected isolates of Enterobacter cloacae and clinical data related to biotype, phage type, O-serotype, and ribotype.

In order to evaluate if ribotyping of selected isolates of Enterobacter cloacae could further elucidate the epidemiology, we performed ribotyping of 109 isolates indistinguishable by bio-, phage-, and O-serotyping, with inconclusive typing results, or from patients with more than one isolate. Ribotyping provided additional information, and some cases of cross-infection or common source of infection were revealed. Under the supposition that isolates sharing the same ribotype were of the same origin, problems arose with respect to bio-, O-sero, as well as phage typing; in particular a remarkable number of isolates showed differences in phage type. In order to identify possible virulence characteristics of certain types, clinical data were related to bio-, phage-, O-sero-, and ribotype. Biotype 66 was significantly more frequent among blood culture isolates (P = 0.001), but this might have reflected the presence of a certain strain in the environment of the intensive care unit, where patients were more likely to develop bacteraemia; serotype 04 was significantly more frequent among isolates from the urinary tract (P = 0.02), and serotype 013 was more frequent among women (P = 0.05). One ribotype was found only among community-acquired isolates, which might suggest that it is a frequent but less virulent strain.

Bacteriophages↗
PubMed1994

Resistance characteristics of blood culture isolates of Enterobacter cloacae with special reference to beta-lactamases and relation to preceding antimicrobial therapy.

Resistance characteristics of 53 blood culture isolates of E. cloacae were examined and correlated with antimicrobial treatment preceding bacteraemia. Resistance patterns of 22 antimicrobial agents, presence of resistant mutants, and inducibility of beta-lactamase were investigated; furthermore, population analysis and investigation of beta-lactamase production of selected isolates were performed. Thirty-two isolates (60%) were resistant to cephalothin and/or cefoxitin and/or ampicillin, and 14 isolates (26%) had further resistance characteristics, 7 of the 14 being resistant to non-beta-lactam antibiotics. All ampicillin-susceptible and 76% of cefotaxime-susceptible isolates had resistant mutants in the zone of inhibition when high inoculum was used. All isolates investigated had inducible chromosomal beta-lactamases, and, in addition, two isolates had an enzyme corresponding with TEM-1. Correlation of resistance patterns and antimicrobial treatment preceding bacteraemia showed that treatment with a third-generation cephalosporin was associated with beta-lactam multiresistance. In conclusion, susceptibility testing of beta-lactam antibiotics of Enterobacter must be interpreted with caution and monotherapy with an extended-spectrum cephalosporin should be avoided unless presence of resistant mutants and inducibility of beta-lactamase can be excluded.

Ampicillin Resistance↗
PubMed1994

Separation and quantification of murein and precursors from Enterobacter cloacae after treatment with trimethoprim and sulphadiazine.

The intracellular concentrations of the soluble murein precursors UDP-Mur-NAc-pentapeptide in the cytoplasm, the membrane-bound lipid precursor disaccharide pentapeptide and the muropeptides of Enterobacter cloacae cultures treated with trimethoprim (12.5 micrograms mL-1) and sulphadiazine (250 micrograms mL-1) were determined by using capillary zone electrophoresis analysis. In the presence of trimethoprim, UDP-Mur-NAc-pentapeptide as well as disaccharide pentapeptide accumulated. In the case of sulphadiazine-treated cells, the concentration of UDP-Mur-NAc-pentapeptide roughly paralleled the control cells but sulphadiazine caused a slow incremental accumulation of disaccharide pentapeptide. The muropeptide composition of the murein indicated that the differences between the peptidoglycans produced by the control cells and the cells grown in the presence of either trimethoprim or sulphadiazine alone or in combination were quite marked. The results suggest that the enhanced activity of trimethoprim plus sulphadiazine against E. cloacae is caused by an additional effect on the inhibition of the bacterial peptidoglycan biosynthesis and that this additional effect is a fundamental part of the antibacterial action of the antimetabolites. This effect leads to changes of cell morphology and resultant changes in bacterial cell permeability.

Carbohydrate Sequence↗
PubMed1990

[Nosocomial infection by new quinolone resistant Enterobacter cloacae].

For the past two years, five strains of new quinolone resistant Enterobacter cloacae have been isolated from three patients in our hospital; strain A was isolated from patient A, strain B from patient B, and strains C1, C2, C3 from patient C. These five strains were resistant to new quinolones and other antimicrobial agents including ampicillin, piperacillin, methicillin, cefotaxime, cefoperazone, kanamycin, gentamicin, tetracycline, minocycline, and chloramphenicol. Plasmid DNA profiles on agarose gel indicated that strain B and C3 carried completely the same plasmid pattern, but strain A gave a different plasmid pattern. Furthermore chromosomal DNAs extracted from strains A, B and C3 were digested with restriction endonucleases EcoR I, BamH I and Sma I. They were separated by pulsefield gel electrophoresis. The banding profiles of strains B and C3 showed the same pattern. It is, therefore, highly suggested that strains B and C3 are the same E. cloacae strain, although isolated from different patients at different time. The possible route of nosocomial infection between these two patients who were hospitalized in the same room after an interval of 4 months was discussed.

4-Quinolones↗
PubMed1997

[Study of septicemia due to Enterobacter cloacae in a neonatal intensive care unit].

A study was made of Enterobacter cloacae septicemia in 15 newborns in the neonatal intensive care unit (NICU) of the Asahikawa Kosei Hospital from April, 1979 to March, 1996. Their gestational age was 29.7 +/- 4.5 (mean +/- SD) weeks and their birth weight was 1,270 +/- 562 g. The age at the onset of septicemia was 10.3 +/- 7.2 days. Four infants died and the mortality was 26.7%. These infants died within 72 hours after onset of septicemia. Thrombocytopenia (< 50,000/microliter) in the patients who died was significantly more than in the patients who improved (p < 0.05). Antibiotic susceptibilities were determined by the Kirby-Bauer method. Three E. cloacae strains isolated in 1982 were sensitive to ampicillin (ABPC) and cefotaxime (CTX), 4 strains between 1983 and 1984 were resistant to ABPC and were sensitive to CTX, 5 strains between 1985 and 1992 were resistant to ABPC and CTX, and 3 strains between 1993 and 1995 were resistant to ABPC and were sensitive to CTX. These results suggested that the emergence of resistant E. cloacae was related to the use of corresponding antibiotics. Our observations showed that E. cloacae was one of the potential pathogens seen in nosocomial infections which is becoming progressively common in newborns and routine bacteriological surveillance is very important in the NICU.

Bacteremia↗
PubMed2006

In vivo reversion to the wild-type beta-lactam resistance phenotype mediated by a plasmid carrying ampR and qnrA1 in Enterobacter cloacae.

Resistance to beta-lactams and quinolones in two isogenic Enterobacter cloacae isolates was studied. One was susceptible to cefoxitin and amoxicillin-clavulanate. The other one showed its natural beta-lactam resistance pattern. Both isolates had a nonfunctional AmpR regulator. However, within the second one, the presence of a plasmid carrying ampR and qnrA1 allowed reversion to the wild-type beta-lactam resistance phenotype and decreased susceptibility to fluoroquinolones.

Amoxicillin-Potassium Clavulanate Combination↗
PubMed2006

Outer membrane protein changes and efflux pump expression together may confer resistance to ertapenem in Enterobacter cloacae.

We investigated ertapenem-susceptible and -resistant extended-spectrum beta-lactamase-producing Enterobacter cloacae isolates obtained from the same patient. Gene transcription of OmpD and OmpF was diminished in the ertapenem-resistant isolate. An efflux pump inhibitor decreased the MICs of ertapenem in the resistant strain, suggesting a potential role of efflux pumps in ertapenem resistance.

Anti-Bacterial Agents↗
PubMed1972

Relation of beta-lactamase activity and cellular location to resistance of Enterobacter to penicillins and cephalosporins.

The Enterobacter species E. aerogenes, E. cloacae, and E. hafnia were examined for resistance to penicillin and cephalosporin derivatives. All were resistant to benzyl penicillin, ampicillin, 6 [d(-)alpha-amino-p-hydroxyphenylacetamido] penicillanic acid, cephaloridine, cephalothin, and cephalexin. A significant number were sensitive to carbenicillin and 6 [d(-)alpha-carboxy-3-thienylacetamido] penicillanic acid. No differences among the three species were noted. The beta-lactamase activity was cell-bound, and was not released by osmotic shock, toluene treatment, or diphenylamine treatment. It was rarely released into the growth medium. The beta-lactamase activity was primarily directed against cephalosporin derivatives. Synthesis of beta-lactamase was chromosomally mediated. Resistance to ampicillin seemed to be partly related to entry of the molecule into the bacteria since exposure to ethylenediaminetetraacetate lowered the minimal inhibitory concentration.

Amidohydrolases↗
PubMed1979

Competition of beta-lactam antibiotics for the penicillin-binding proteins of Pseudomonas aeruginosa, Enterobacter cloacae, Klebsiella aerogenes, Proteus rettgeri, and Escherichia coli: comparison with antibacterial activity and effects upon bacterial morphology.

The competition of a number of beta-lactam morphogenic probes for the penicillin-binding proteins (PBPs) of Pseudomonas aeruginosa, Enterobacter cloacae, Klebsiella aerogenes, Proteus rettgeri, and Escherichia coli has been studied. The results indicate that the various gram-negative bacteria have similar, but not identical, PBP patterns and that the individual proteins probably perform similar morphogenic functions as in E. coli K-12. Comparison of the 50% binding concentrations of the compounds for the various PBPs of the five strains with their antibacterial activity indicates that the different antibiotics are excluded to a greater or lesser degree by the outer membrane permeability barrier and that the exclusion is most pronounced in P. aeruginosa.

Anti-Bacterial Agents↗