Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Enterobacter”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 523 records · Page 29Linked to original sources
PubMed2000

Enterobacter cloacae bloodstream infections traced to contaminated human albumin.

In August 1996, a patient in Kansas developed an Enterobacter cloacae bloodstream infection (BSI) shortly after receiving Albuminar, a brand of human albumin. Albuminar contamination was suspected. A case-control study of patients with primary gram-negative bacterial BSIs showed that patients with E. cloacae BSIs were significantly more likely than patients with non-E. cloacae gram-negative BSIs to have received Albuminar within 3 days of developing their BSIs (3 of 5 vs. 0 of 9; OR, undefined; P=.03). The E. cloacae isolate from the Kansas patient was found by pulsed-field gel electrophoresis to be identical to the isolate from the patient's Albuminar vial, to isolates from 2 previously unopened Albuminar vials, and to an isolate from a Wisconsin patient who had received Albuminar. A worldwide recall of approximately 116,000 Albuminar vials took place. This multistate outbreak was detected because of clinical astuteness and prompt reporting. Combined epidemiological and laboratory approaches are valuable when investigating potentially contaminated blood components and plasma derivatives.

Adult↗
PubMed2002

Regional occurrence of plasmid-mediated SHV-7, an extended-spectrum beta-lactamase, in Enterobacter cloacae in Philadelphia Teaching Hospitals.

Although the production of extended-spectrum beta-lactamases (ESBLs) by Klebsiella pneumoniae and Escherichia coli is an emerging problem, limited data are available regarding the frequency of ESBL production in other organisms. We provide the only description of regional occurrence of SHV-7 in Enterobacteriaceae other than E. coli or K. pneumoniae in the United States, and we emphasize that, among Enterobacter cloacae strains, not all resistance to extended-spectrum cephalosporins is the result of hyperproduction of AmpC beta-lactamase.

Bacterial Proteins↗
PubMed1999

Outbreak of Enterobacter cloacae related to understaffing, overcrowding, and poor hygiene practices.

OBJECTIVE: To determine the cause and mode of transmission of a cluster of infections due to Enterobacter cloacae. DESIGN AND SETTING: Retrospective cohort study in a neonatal intensive-care unit (NICU) from December 1996 to January 1997; environmental and laboratory investigations. SUBJECTS: 60 infants hospitalized in the NICU during the outbreak period. MAIN OUTCOME MEASURES: Odds ratios (OR) linking E. cloacae colonization or infection and various exposures. All available E. cloacae isolates were typed and characterized by contour-clamped homogenous electric-field electrophoresis to confirm possible cross-transmission. RESULTS: Of eight case-patients, two had bacteremia; one, pneumonia; one, soft-tissue infection; and four, respiratory colonization. Infants weighing <2,000 g and born before week 33 of gestation were more likely to become cases (P<.001). Multivariate analysis indicated that the use of multidose vials was independently associated with E. cloacae carriage (OR, 16.3; 95% confidence interval [CI95], 1.8-infinity; P=.011). Molecular studies demonstrated three epidemic clones. Cross-transmission was facilitated by understaffing and overcrowding (up to 25 neonates in a unit designed for 15), with an increased risk of E. cloacae carriage during the outbreak compared to periods without understaffing and overcrowding (relative risk, 5.97; CI95 2.2-16.4). Concurrent observation of healthcare worker (HCW) handwashing practices indicated poor compliance. The outbreak was terminated after decrease of work load, increase of hand antisepsis, and reinforcement of single-dose medication. CONCLUSIONS: Several factors caused and aggravated this outbreak: (1) introduction of E. cloacae into the NICU, likely by two previously colonized infants; (2) further transmission by HCWs' hands, facilitated by substantial overcrowding and understaffing in the unit; (3) possible contamination of multidose vials with E. cloacae. Overcrowding and understaffing in periods of increased work load may result in outbreaks of nosocomial infections and should be avoided.

Cross Infection↗
PubMed2000

A heterogeneous outbreak of Enterobacter cloacae and Serratia marcescens infections in a surgical intensive care unit.

OBJECTIVE: To investigate an outbreak of invasive disease due to Enterobacter cloacae and Serratia marcescens in a surgical intensive care unit (ICU). DESIGN: Pulsed-field gel electrophoresis (PFGE) analysis of restriction fragments was used to characterize the outbreak isolate genotypes. A retrospective cohort study of surgical ICU patients was conducted to identify risk factors associated with invasive disease. Unit staffing data were analyzed to compare staffing levels during the outbreak to those prior to and following the outbreak. SETTING: An urban hospital in San Francisco, California. PATIENTS: During the outbreak period, December 1997 through January 1998, there were 52 patients with a minimum ICU stay of > or = 72 hours. Of these, 10 patients fit our case definition of recovery of E. cloacae or S. marcescens from a sterile site. RESULTS: PFGE analysis revealed a highly heterogeneous population of isolates. Bivariate analysis of patient-related risk factors revealed duration of central lines, respiratory colonization, being a burn patient, and the use of gentamicin or nafcillin to be significantly associated with invasive disease. Both respiratory colonization and duration of central lines remained statistically significant in a multivariate analysis. Staffing data suggested a temporal correlation between understaffing and the outbreak period. CONCLUSIONS: Molecular epidemiological techniques provided a rapid means of ruling out a point source or significant cross-contamination as modes of transmission. In this setting, patient-related risk factors, such as respiratory colonization and duration of central lines, may provide a focus for heightened surveillance, infection control measures, and empirical therapy during outbreaks caused by common nosocomial pathogens. In addition, understaffing of nurses may have played a role in this outbreak, highlighting the importance of monitoring staffing levels.

Cohort Studies↗
PubMed2002

Risk factors for infection and molecular typing in patients in the intensive care unit colonized with nosocomial Enterobacter aerogenes.

OBJECTIVES: To determine the frequency of colonization by Enterobacter aerogenes in patients in the intensive care unit (ICU) for more than 48 hours and to evaluate the risk factors for infection in patients colonized by this bacteria. DESIGN: An 8-month prospective study. SETTING: A 12-bed medical-surgical ICU in a 450-bed, university-affiliated, tertiary-care hospital in Belgium. METHOD: Pulsed-field gel electrophoresis was used to determine the genotypes of E. aerogenes isolates. RESULTS: We observed two major clones of E. aerogenes in the ICU. Interestingly, 87.5% of infected patients had the same genomic profile for colonization and infection. Risk factors for infection in this particular population included younger age, prolonged hospital stay, mechanical ventilation, and bronchoscopy. CONCLUSIONS: Colonization is a major prerequisite for infection. The identification of risk factors for infection in colonized patients can optimize the quality of treatment in the ICU.

Aged↗
PubMed2003

Meningitis due to Enterobacter aerogenes subsequent to resection of acoustic neuroma and percutaneous endoscopic gastrostomy tube placement: a rare nosocomial event.

We present a case of meningitis after percutaneous endoscopic gastrostomy (PEG) tube placement subsequent to acoustic neuroma resection and cranioplasty. Four days following PEG tube placement, the patient developed Enterobacter aerogenes meningitis, requiring explantation of infected cranioplasty material. His condition subsequently improved. Etiology and future intervention strategies are discussed.

Adult↗
PubMed2003

Molecular epidemiology of systemic infection caused by Enterobacter cloacae in a high-risk neonatal intensive care unit.

OBJECTIVE: To investigate the molecular epidemiology of systemic nosocomial infections caused by Enterobacter cloacae. SETTING: Neonatal intensive care unit (NICU) of a tertiary-care university hospital. PATIENTS: Forty-two high-risk neonates with systemic infections caused by E. cloacae. METHODS: From 1995 to 1997, the variables associated with death in these patients were evaluated. The molecular epidemiology of the strains responsible for the systemic infections, and 14 unrelated strains, was studied using plasmid analysis and pulsed-field gel electrophoresis (PFGE). RESULTS: The overall mortality rate for infection caused by E. cloacae was 34%, whereas the crude mortality rate during the study period was 8.12% (P < .001). Gestational age (preterm neonates) and birth weight (small for gestational age) were not associated with a higher risk of death. Insertion of a venous catheter by dissection of a peripheral vein was the only invasive procedure related to death (P = .016) in this study. A molecular analysis showed that three outbreaks, each occurring in a different year, were caused by strains with distinctive DNA profiles. Only one outbreak was identified by the infection control service, in the NICU. Plasmid analysis and PFGE showed similar ability to discriminate control strains from the E. cloacae strains isolated from the neonates. CONCLUSIONS: Systemic infections caused by E. cloacae in our NICU were associated with a high mortality rate and occurred as small, unrecognized outbreaks. These results may not be generalizable because the data were from a single center.

Bacterial Typing Techniques↗
PubMed1997

An outbreak of Enterobacter hormaechei infection and colonization in an intensive care nursery.

Enterobacter hormaechei was first identified as a unique species in 1989. Between 29 November 1992 and 17 March 1993, an outbreak of E. hormaechei occurred among premature infants in the intensive care nursery (ICN) at The Hospital of the University of Pennsylvania. The 10 infants whose cultures were positive for E. hormaechei (six were infected and four were colonized) had a lower median estimated gestational age and birth weight than did other ICN infants; other risk factors for infection or colonization with E. hormaechei were not identified. Cultures from three isolettes and a doorknob in the ICN were positive for E. hormaechei. Pulsed-field gel electrophoresis of isolates from six patients and two isolettes were identical. Observations of health care workers revealed breaks in infection control techniques that may have allowed transmission of this organism. We found that E. hormaechei is a nosocomial pathogen that can infect vulnerable hospitalized patients and that can be transmitted from patient to patient when infection control techniques are inadequate.

Disease Outbreaks↗
PubMed1998

Induction of beta-lactamase in Enterobacter cloacae.

beta-lactamase induction in Enterobacter cloacae, which is linked to peptidoglycan recycling, was investigated with use of high-performance liquid chromatography of cell wall fragments in genetically defined cells of Escherichia coli. After treatment of cells with beta-lactams, we detected in the periplasm an increase of D-tripeptide (N-acetylglucosaminyl-1,6 anhydro N-acetylmuramyl-L-alanyl-D-glutamyl-meso-diaminopimelic acid), D-tetrapeptide (N-acetylglucosaminyl-1, 6 anhydro N-acetylmuramyl-L-alanyl-D-glutamyl-meso-diaminopimelic acid -D-alanine), and a yet-unknown anhydromuropeptide. We identified this anhydromuramylpeptide by fast atom bombardment-mass spectrometry as anhydromuramyl-pentapeptide. The amount of these molecules did not alter after treatment with cell wall-active non beta-lactams. The transmembrane protein AmpG transports not only D-tripeptide but also D-pentapeptide into the cell. In the cytoplasm these molecules are degraded into the corresponding monosaccharide peptides M-tripeptide (N-acetylmuramyl-L-alanyl-D-glutamyl-meso-diaminopimelic acid) and M-pentapeptide (N-acetylmuramyl-L-alanyl-D-glutamyl-meso-diaminopimelic acid-alanine-D-alanine). These findings indicate that besides M-tripeptide and D-tripeptide, probably M-tetrapeptide, D-tetrapeptide, M-pentapeptide, and D-pentapeptide are also signal muropeptides for beta-lactamase induction.

Bacterial Proteins↗
PubMed1995

Interrepeat fingerprinting of third-generation cephalosporin-resistant Enterobacter cloacae isolated during an outbreak in a neonatal intensive care unit.

OBJECTIVE: To investigate an outbreak in neonates of Enterobacter cloacae infection resistant to third-generation cephalosporins. DESIGN: A retrospective study of an outbreak in the neonatal intensive care unit (NICU) and review of E cloacae isolates in pediatric wards and other intensive care units from June 1992 through March 1993. SETTING: An academic tertiary care hospital. PATIENTS: Six patients admitted to the NICU were colonized or infected with E cloacae resistant to third-generation cephalosporins. In the period preceding the outbreak, four E cloacae isolates were available from four patients in the pediatric surgical ward. Nine isolates from four patients in two other intensive care units (ICUs) also were collected during the outbreak. Isolates were biotyped by the API 50CH system and genotyped by polymerase chain reaction (PCR) fingerprinting. RESULTS: Typing by interrepeat PCR showed that 21 isolates, which were obtained from five neonates, were identical. One neonate was colonized with a different strain. Some neonates were colonized with a single type of E cloacae for a relatively long period of time. Isolates of patients who were cared for in the pediatric surgical ward and the two other intensive care units (ICUs) showed different genotypes. One patient in an ICU was colonized with an E cloacae strain genetically identical to the outbreak strain. No predominant biotype could be established. CONCLUSIONS: E cloacae can colonize neonates for a long period of time and although colonization with E cloacae initially may arise endogenously, we were able to show further transmission by cross-contamination in a neonatal intensive care unit.

Bacterial Typing Techniques↗
PubMed1995

Characterization of nosocomial strains of Enterobacter aerogenes by arbitrarily primed-PCR analysis and ribotyping.

OBJECTIVE: To study the spread of strains of Enterobacter aerogenes in our hospital in 1992 and 1993 by using two genotypic markers, and to evaluate these methods for the epidemiological investigation of this species. DESIGN: Ribotyping (using two endonucleases) and arbitrarily primed (AP)-PCR (using two different 10-mer primers) were applied to the epidemiological typing of clinical strains of E aerogenes isolated from hospitalized patients. SETTING AND PATIENTS: The intensive care unit (ICU; 5 patients, 13 isolates), nephrology units (3 patients, 5 isolates), and surgery units (2 patients, 2 isolates) of the university hospital of Saint-Etienne (France). RESULTS: Eight epidemiologically unrelated isolates, chosen as controls, exhibited distinct profiles, both by AP-PCR and ribotyping. Two clones of E aerogenes circulated in the ICU; both were isolated successively from samples of a single patient who stayed in the unit for almost 1 year. A third clone was recovered from patients of surgery units. A fourth clone was shown to have infected patients of nephrology units. CONCLUSIONS: Ribotyping and AP-PCR appear to be reliable methods for typing E aerogenes strains implicated in nosocomial infection. The spread of independent clones of E aerogenes in different units of our hospital in 1992 and 1993 was demonstrated by both methods. This study emphasizes the need to choose the endonucleases or primers with care to obtain high discriminatory results in genotypic investigations.

Bacterial Typing Techniques↗
PubMed1997

Ribotyping and random amplification of polymorphic DNA for nosocomial Enterobacter cloacae isolates in a pediatric intensive-care unit.

Between 1987 and 1989, two sequential outbreaks of nosocomial infection caused by Enterobacter cloacae occur-red in the pediatric intensive-care unit of a tertiary-care teaching hospital. Seventeen strains retrieved from the outbreaks and two control strains identified in other wards were typed by ribotyping and random amplification of polymorphic DNA (RAPD). The results indicated that the genomic pattern of strains identified between the first and second outbreaks was different. We conclude that both ribotyping and RAPD are highly discriminatory and reproducible methods for typing E cloacae. RAPD seems to be more efficacious and cost-effective.

Bacterial Typing Techniques↗
PubMed1978

Standardization of a rapid microbiologic assay for aminoglycosides using Enterobacter cloacae.

The standardization of a rapid serum aminoglycoside assay using Enterobacter cloacae is described. This includes the sensitivity testing of the organism and its performance on various media, with Mueller-Hinton agar being the medium of choice. The precision and reproducibility of the assay, as measured by the within-run and between-run coefficients of variation, were 5.0 and 5.9, respectively. A significant positive correlation was obtained between the microbiologic assay for gentamicin and a 125I-labeled gentamicin radioimmunoassay with the use of both normal and uremic sera. When known amounts of gentamicin, tobramycin, and amikacin were added to antibiotic-free sera from normal persons, recovery rates of 80.0% to 97.9% were found. In the case of gentamicin, recovery rates of 85.0% to 97.9% were found with the use of sera from patients undergoing either hemodialysis or peritoneal dialysis. There were no effects on the recovery rates of the aminoglycosides from normal serum if high concentrations of clindamycin, methicillin, ampicillin, penicillin G, cephalothin, cefamandole or cefoxitin were also present in the sera. The newer cephalosporins, cefamandole and cefoxitin, had no in-vitro effect on the Kirby-Bauer sensitivity patterns of gentamicin, tobramycin, or amikacin, when tested against the assay organism.

Agar↗
PubMed1980

A biotype of Enterobacteriaceae intermediate between Citrobacter and Enterobacter.

The authors isolated two strains of an unnamed bacterial biotype with characteristics intermediate between those of Enterobacter and Citrobacter. The organisms did not produce acetyl-methyl carbinol, but decarboxylated lysine. Apart from the latter trait, they most closely resemble H2S-negative Citrobacter freundii. They differ biochemically from all other currently accepted species of enterobacteriaceae. Their pathogenic significance appears similar to that of the two genera they most closely resemble. Only by recognition and study of additional strains can their identity be more definitively delineated and their significance more fully assessed.

Child↗
PubMedDate not supplied

Biochemical characterization of type A and type B beta-lactamase from Enterobacter cloacae.

Different types of chromosomally coded beta-lactamases are found in Enterobacter cloacae. E. cloacae M6300 produces beta-lactamase type A, which has an isoelectric point of 8.8, whereas E. cloacae 908 R produces beta-lactamase type B, which has an isoelectric point of 7.9. Both enzymes were purified to homogeneity by a procedure that included affinity chromatography on amino phenylboronic acid-modified Sepharose. The two enzymes were closely related as shown by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, kinetic constants with several substrates, amino acid composition, NH2-terminal amino acid sequence, and reaction with antisera. In addition to having different isoelectric points, the two enzymes migrated to slightly different positions on polyacrylamide gels and differed significantly in rate of catalysis for cephalothin, imipenem, and the penem Sch 34343. One of three antisera seemed to recognize an epitope that differs in the two enzymes. The diversity of cephalosporinases found in E. cloacae with respect to the evolution of novel beta-lactamases was considered.

Amino Acid Sequence↗
PubMedDate not supplied

Genetic control of beta-lactamase production in Enterobacter cloacae.

In Enterobacter cloacae, mutations in favor of overproduction of beta-lactamase--leading to resistance to third-generation cephalosporins--occur at frequencies of 10(-4)-10(-7). Cloning experiments reveal that at least three genes are involved in the regulation of chromosomal beta-lactamase expression. The structural gene, ampC, is located adjacent to the regulatory gene, ampR, coding for a protein that can serve as an activator in the presence of an inducer. An example of an ampR mutant that is independent of an inducer has been studied. More important for the development of cefotaxime resistance in E. cloacae are mutations in the ampD gene and other proposed regulatory genes. Inactivation of the ampD gene leads to elevated beta-lactamase production. Thus, ampD negatively controls ampC expression. Evidence for the existence of a third regulatory gene, ampE, has been found.

Cloning, Molecular↗
PubMedDate not supplied

Impact of the ampD gene and its product on beta-lactamase production in Enterobacter cloacae.

In an investigation of the influence of the ampD gene on beta-lactamase production and induction in Enterobacter cloacae, the ampR-ampC gene region cloned into a plasmid and the ampD gene cloned into another vector were transferred to a strain of Escherichia coli. The genetically manipulated E. coli strains served as a model for study of the inducibility of beta-lactamases in E. cloacae. In addition, beta-lactamase induction in E. cloacae bearing the previously mentioned plasmids was studied. After induction of the beta-lactamase with cefoxitin, the specific hydrolytic activity, the viable cell count, and the degradation of cefoxitin were determined. beta-Lactamase expression decreased with an increasing amount of the ampD gene product. The cefoxitin concentration decreased in proportion to the amount of enzyme, but the induction of beta-lactamase seemed not to be an important factor influencing the viable cell count of E. cloacae as long as cefoxitin concentrations exceeded the MIC. Despite different beta-lactamase concentrations, the decrease in the viable cell count was nearly identical in all experiments.

Cefoxitin↗