Enterobacter cloacae: Bacteremia, Epidemiology, and Antibiotic Resistance

John, Joseph F.; Sharbaugh, Robert J.; Bannister, Edward R.

doi:10.1093/clinids/4.1.13

Cited by 105 publications

(72 citation statements)

References 85 publications

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“…pQC provides outbreak strains with a greater likelihood of survival in the hospital environment. This refutes the hypothesis of the early 1980s that expressed the hope that 'new agents' such as cefotaxime and cefoperazone eventually may be valuable for single-drug therapy of infections due to E. cloacae (John et al, 1982).…”

Section: Discussionsupporting

confidence: 51%

Identification of resistance and virulence factors in an epidemic Enterobacter hormaechei outbreak strain

Paauw

Caspers²,

Hall

et al. 2009

Microbiology

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Bacterial strains differ in their ability to cause hospital outbreaks. Using comparative genomic hybridization, Enterobacter cloacae complex isolates were studied to identify genetic markers specific for Enterobacter cloacae complex outbreak strains. No outbreak-specific genes were found that were common in all investigated outbreak strains. Therefore, the aim of our study was to identify specific genetic markers for an Enterobacter hormaechei outbreak strain (EHOS) that caused a nationwide outbreak in The Netherlands. Most EHOS isolates carried a large conjugative plasmid (pQC) containing genes encoding heavy-metal resistance, mobile elements, pili-associated proteins and exported proteins as well as multiple-resistance genes. Furthermore, the chromosomally encoded high-pathogenicity island (HPI) was highly associated with the EHOS strain. In addition, other DNA fragments were identified that were associated with virulence: three DNA fragments known to be located on a virulence plasmid (pLVPK), as well as phage-and plasmid-related sequences. Also, four DNA fragments encoding putative pili with the most homology to pili of Salmonella enterica were associated with the EHOS. Finally, four DNA fragments encoding putative outer-membrane proteins were negatively associated with the EHOS. In conclusion, resistance and putative virulence genes were identified in the EHOS that may have contributed to increased epidemicity. The high number of genes detected in the EHOS that were related to transferable elements reflects the genomic plasticity of the E. cloacae complex and may explain the emergence of the EHOS in the hospital environment. INTRODUCTIONIn the pre-antibiotic era, isolates of the Enterobacter cloacae complex were not detected in surveys of nosocomial bacteria; they were first described as nosocomial pathogens in the 1970s (Sanders & Sanders, 1997). In 2001, Enterobacter spp. caused 7 % of nosocomial infections in intensive care units in the USA (Jones, 2003;Streit et al., 2004). Therefore, the E. cloacae complex can be considered as an emerging pathogen, of which Enterobacter hormaechei is the most commonly isolated nosocomial pathogen (Delmas et al., 2006;Paauw et al., 2008). A nationwide outbreak occurred with an E. hormaechei outbreak strain (EHOS) in The Netherlands . This strain disseminated throughout hospitals despite adequate implementation of internationally accepted infection-prevention guidelines and caused invasive infections in more than 100 patients (Paauw et al., 2007). Previous studies showed that most EHOS isolates carried the conjugative plasmid pQC, with several complex integrons containing aadB, bla CTX-M-9 and qnrA1 genes that encoded resistance to aminoglycosides and thirdgeneration cephalosporins, and reduced susceptibility to fluoroquinolones, respectively . However, it was also shown that other Enterobacteriaceae including other E. cloacae complex isolates with the pQC did not become highly epidemic like the EHOS (Paauw et al., 2007). Furthermore, of aminoglycoside-susceptible E. cloa...

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Section: Discussionsupporting

confidence: 51%

Identification of resistance and virulence factors in an epidemic Enterobacter hormaechei outbreak strain

Paauw

Caspers²,

Hall

et al. 2009

Microbiology

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“…A large plasmid was detected in strain EM, while no plasmid was found in the reference strain E. The plasmid in strain EM was extracted and purified by CsCl gradient centrifugation, and its molecular size was estimated at 100 Ϯ 20 kb. High-molecular-weight plasmids were previously found in E. cloacae isolates from nosocomial infections that had a high level of multiresistance (14,22). Transfer of the plasmid from strain EM by transformation of strains E. cloacae E and of E. coli XL1-Blue did not yield transformants able to hydrolyze crystallized parabens on tryptic soy agar.…”

Section: Resultsmentioning

confidence: 95%

Hydrolysis of 4-Hydroxybenzoic Acid Esters (Parabens) and Their Aerobic Transformation into Phenol by the Resistant Enterobacter cloacae Strain EM

Valkova

Lépine

Valeanu

et al. 2001

Appl Environ Microbiol

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Enterobacter cloacae strain EM was isolated from a commercial dietary mineral supplement stabilized by a mixture of methylparaben and propylparaben. It harbored a high-molecular-weight plasmid and was resistant to high concentrations of parabens. Strain EM was able to grow in liquid media containing similar amounts of parabens as found in the mineral supplement (1,700 and 180 mg of methyl and propylparaben, respectively, per liter or 11.2 and 1.0 mM) and in very high concentrations of methylparaben (3,000 mg liter ؊1 , or 19.7 mM). This strain was able to hydrolyze approximately 500 mg of methyl-, ethyl-, or propylparaben liter ؊1 (3 mM) in less than 2 h in liquid culture, and the supernatant of a sonicated culture, after a 30-fold dilution, was able to hydrolyze 1,000 mg of methylparaben liter ؊1 (6.6 mM) in 15 min. The first step of paraben degradation was the hydrolysis of the ester bond to produce 4-hydroxybenzoic acid, followed by a decarboxylation step to produce phenol under aerobic conditions. The transformation of 4-hydroxybenzoic acid into phenol was stoichiometric. The conversion of approximately 500 mg of parabens liter ؊1 (3 mM) to phenol in liquid culture was completed within 5 h without significant hindrance to the growth of strain EM, while higher concentrations of parabens partially inhibited its growth.

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“…ODC-E. cloacae had been previously rare in this hospital, (11,14,17). Their chromosomal beta-lactamase genes (25) make them resistant to the cephalosporins used widely in this burn unit (Tables 3 and 4).…”

Section: Resultsmentioning

confidence: 99%

Molecular evolution, species distribution, and clinical consequences of an endemic aminoglycoside resistance plasmid

Mayer¹,

Hopkins²,

Gilleece³

et al. 1986

Antimicrob Agents Chemother

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During the first 6 years after appearing in one hospital, a 92-kilobase conjugative plasmid, pBWHl, which encoded resistance to chloramphenicol and sulfonamides and determined TEM-1 beta-lactamase and 2"-aminoglycoside nucleotidyltransferase, underwent a variety of molecular changes. It was most prevalent initially in isolates of Klebsiella pneumoniae, then in isolates of Serratia marcescens, and finally, after nearly disappearing, in isolates of Enterobacter cloacae. Evolutionary changes in the plasmid did not account for its shifts in species distribution, since the original molecule was found in isolates of each species. The late resurgence of pBWHl occurred after a copy of its original molecule entered a distinctive ornithine decarboxylase-negative strain of E. cloacae, new to the hospital. The resulting transconjugant strain, chromosomally resistant to topical silver salts and to cephalosporins, and with the addition of pBWH1-encoded aminoglycoside resistance, spread in the hospital by causing an outbreak of sepsis in the burn unit, where these were commonly used antibacterial agents. Thus, an endemic plasmid became prevalent in a new host species because one of its genes supplemented the fitness of an uncommon strain of the species for a particular clinical niche.The percentages of clinical isolates of different bacterial species resistant to specific antibiotics are frequently calculated to delineate the usefulness of these drugs. Such tabulations will reflect in large part the distribution of resistance plasmids among strains of the species being surveyed, since a majority of resistance genes are carried by plasmids (4). The distribution of the plasmids may be determined by properties of the plasmids themselves such as their transferability, host range, or stability or the selective advantages conferred by their resistance genes or other cryptic genes (4,5). Also, properties of the host strains such as their fitness to occupy niches in which they come in contact with antibiotics might contribute to the observed distribution of plasmids.The surveillance of antibiotic resistance plasmids has been aided by plasmid fingerprinting, using restriction endonucleases (6,9,10,15,24,27)

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Enterobacter cloacae: Bacteremia, Epidemiology, and Antibiotic Resistance

Cited by 105 publications

References 85 publications

Identification of resistance and virulence factors in an epidemic Enterobacter hormaechei outbreak strain

Identification of resistance and virulence factors in an epidemic Enterobacter hormaechei outbreak strain

Hydrolysis of 4-Hydroxybenzoic Acid Esters (Parabens) and Their Aerobic Transformation into Phenol by the Resistant Enterobacter cloacae Strain EM

Molecular evolution, species distribution, and clinical consequences of an endemic aminoglycoside resistance plasmid

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