# Enterobacter
**Enterobacter** is a genus of Gram-negative, aerobic, motile bacteria in the family [Enterobacteriaceae](https://www.edgepedia.org/enterobacteriaceae), best known as opportunistic nosocomial pathogens and for inducible antibiotic resistance.[1](https://www.frontiersin.org/journals/microbiology/articles/10.3389/fmicb.2023.1122691/full) The genus belongs to the ESKAPE group of [Gram-negative bacteria](https://www.edgepedia.org/gram-negative-bacteria) in which dissemination of resistance genes via mobile genetic elements is an important aspect of antibiotic resistance.[2](https://pmc.ncbi.nlm.nih.gov/articles/PMC6750132/) Most clinically important isolates belong to the *Enterobacter cloacae* complex, a set of closely related species that are difficult to tell apart by routine phenotypic methods.[3](https://pmc.ncbi.nlm.nih.gov/articles/PMC2515634/)
| Key fact | Detail |
|---|---|
| Classification | Gram-negative, aerobic, motile bacteria of the family Enterobacteriaceae[1](https://www.frontiersin.org/journals/microbiology/articles/10.3389/fmicb.2023.1122691/full) |
| Main clinical group | *E. cloacae* complex, comprising six species: *E. cloacae*, *E. asburiae*, *E. hormaechei*, *E. kobei*, *E. ludwigii*, and *E. nimipressuralis*[4](https://www.tandfonline.com/doi/full/10.2217/fmb.12.61) |
| Intrinsic resistance | Inducible AmpC β-lactamases not inhibited by β-lactamase inhibitors, causing resistance to ampicillin, co-amoxiclav, and first-generation cephalosporins[5](https://pubmed.ncbi.nlm.nih.gov/15700687/) |
| Carbapenem resistance mechanisms | Carbapenemase production, efflux pumps, and decreased outer membrane permeability through porin mutations[6](https://pmc.ncbi.nlm.nih.gov/articles/PMC6628318/) |
| Colistin resistance | Annual rates of 4.4%–20% among *E. cloacae* complex isolates, with a rising trend among bloodstream organisms, versus generally <2% for *E. coli* and *Klebsiella* spp.[7](https://academic.oup.com/jac/article/75/9/2452/5854852) |
| Species identification | Phenotypic identification is unreliable; multilocus sequence analysis of housekeeping genes is the most valuable tool, and MALDI-TOF mass spectrometry does not distinguish the species[8](https://journals.asm.org/doi/10.1128/CMR.00002-19) |
## Taxonomy and the *E. cloacae* complex
Biochemical and molecular studies have shown that what was once called *E. cloacae* is genomically heterogeneous, comprising six species: *Enterobacter cloacae*, *Enterobacter asburiae*, *Enterobacter hormaechei*, *Enterobacter kobei*, *Enterobacter ludwigii*, and *Enterobacter nimipressuralis*; *E. cloacae* and *E. hormaechei* are the most frequently isolated in human clinical specimens.[4](https://www.tandfonline.com/doi/full/10.2217/fmb.12.61) Isolates of the complex have been increasingly isolated as nosocomial pathogens, but phenotypic identification is unreliable and irreproducible.[3](https://pmc.ncbi.nlm.nih.gov/articles/PMC2515634/)
**Identification methods.** Multilocus sequence analysis (MLSA) employing sequencing of four to seven housekeeping genes, such as *atpD*, *fusA*, *infB*, *gyrB*, *leuS*, *dnaA*, *pyrG*, *rplB*, *rpoB*, and *hsp60*, has appeared as the most valuable tool for identifying *E. cloacae* complex species and the most recent Enterobacter species.[8](https://journals.asm.org/doi/10.1128/CMR.00002-19) [Mass spectrometry](https://www.edgepedia.org/mass-spectrometry) alone does not allow the species to be distinguished from each other, so associations must be established using real-time PCR amplifying the *dnaJ* gene.[8](https://journals.asm.org/doi/10.1128/CMR.00002-19) A species identification error has no impact on antibiotic therapy, because the species of the *E. cloacae* complex have the same antibiotic resistance profiles.[8](https://journals.asm.org/doi/10.1128/CMR.00002-19) Whole-genome sequencing has further refined the classification; one in silico analysis of 1,249 Enterobacter-labeled genomes revealed 22 clades spanning 11 Hoffmann clusters, and suggested that *E. hormaechei* contains at least five subspecies.[9](https://doi.org/10.1128/Spectrum.00661-21)
## Intrinsic and inducible resistance
Enterobacter species produce small amounts of inducible AmpC β-lactamases that are not inhibited by β-lactamase inhibitors, causing intrinsic resistance to ampicillin, co-amoxiclav, and first-generation cephalosporins.[5](https://pubmed.ncbi.nlm.nih.gov/15700687/) AmpC production is low (repressed) or inducible (derepressed, for example following induction with cefoxitin), conferring resistance to aminopenicillins and early-generation cephalosporins such as cephalothin, cefuroxime, and cefoxitin.[10](https://www.mdpi.com/1422-0067/21/14/5090)
AmpC-mediated resistance falls into three categories: inducible chromosomal resistance that emerges in the setting of a β-lactam compound, stable derepression due to mutations in *ampC* regulatory genes, and plasmid-mediated *ampC* genes.[11](https://pubmed.ncbi.nlm.nih.gov/30838380/) Most experts agree it is prudent to avoid expanded-spectrum (third-generation) cephalosporins for organisms posing the greatest risk of *ampC* induction, a risk best described for *Enterobacter cloacae* infections.[11](https://pubmed.ncbi.nlm.nih.gov/30838380/) AmpC β-lactamases are chromosomal and inducible in most *Enterobacter* spp., and the enzymes are resistant to almost all penicillins and cephalosporins, to β-lactamase inhibitors, and to aztreonam, while remaining susceptible to cefepime and carbapenems.[5](https://pubmed.ncbi.nlm.nih.gov/15700687/)
Plasmid-borne AmpC enzymes are more prevalent in *Klebsiella* and *Salmonella* species, whereas class C AmpC β-lactamases in *Enterobacter* and *Citrobacter* species are usually encoded by chromosomal *ampC* genes such as CMY-2, P99, ACT-1, and DHA-1.[10](https://www.mdpi.com/1422-0067/21/14/5090)
## Carbapenem resistance
Enterobacteriaceae employ three primary mechanisms of resistance to carbapenems: enzymatic degradation through carbapenemase production, expression of efflux pumps, and decreased outer membrane permeability via porin mutations.[6](https://pmc.ncbi.nlm.nih.gov/articles/PMC6628318/) The production of extended-spectrum or AmpC β-lactamases alone, without membrane impermeability, is insufficient to confer clinical carbapenem resistance; loss of both major porins or mutations in genes regulating the porin system raise carbapenem resistance substantially.[12](https://pmc.ncbi.nlm.nih.gov/articles/PMC7771540/) Porins tend to have exclusion limits approaching the size of many antibiotics and so limit the rate of diffusion of these molecules, contributing to intrinsic resistance.[13](https://pmc.ncbi.nlm.nih.gov/articles/PMC3485749/)
**Carbapenemases in Enterobacter.** A genomic epidemiology study of carbapenemase-producing Enterobacter spp., comprising predominantly *E. xiangfangensis* and *E. hormaechei* isolates, reported that the most common enzyme identified is VIM, followed by NDM, KPC, OXA-48, and IMP.[2](https://pmc.ncbi.nlm.nih.gov/articles/PMC6750132/) Carbapenem-resistant *E. cloacae* complex has emerged as an important multidrug-resistant pathogen in healthcare settings, although it has historically received less attention than carbapenem-resistant *Klebsiella pneumoniae* and other major carbapenem-resistant Enterobacterales.[14](https://www.mdpi.com/2076-2607/14/3/594)
## Colistin resistance
Polymyxins such as colistin have re-entered use against problem Gram-negative bacteria, and resistance among *E. cloacae* complex isolates proved unexpectedly frequent. Annual colistin resistance rates among *E. cloacae* complex isolates were 4.4%–20%, with a rising trend among bloodstream organisms, while annual rates for *Escherichia coli* and *Klebsiella* spp. (including *K. aerogenes*) generally remained below 2%.[7](https://academic.oup.com/jac/article/75/9/2452/5854852) This resistance is associated with particular genomic and metabolic clusters, identification as *E. asburiae*, and more complex lipopolysaccharide architectures.[7](https://academic.oup.com/jac/article/75/9/2452/5854852)
## Clinical significance
*E. cloacae* complex isolates have been increasingly isolated as nosocomial pathogens.[3](https://pmc.ncbi.nlm.nih.gov/articles/PMC2515634/) Because the species of the complex share the same antibiotic resistance profiles, a species identification error has no impact on antibiotic therapy, even though distinguishing them matters for epidemiology.[8](https://journals.asm.org/doi/10.1128/CMR.00002-19) Regarding quinolones, *Enterobacter cloacae* is one of the enterobacteria, along with *Escherichia coli* and *Klebsiella pneumoniae*, in which plasmid-origin resistance due to the QnrA protein was initially observed.[2](https://pmc.ncbi.nlm.nih.gov/articles/PMC6750132/)
## References
1. [Species identification, antibiotic resistance, and virulence in Enterobacter cloacae complex clinical isolates from South Korea, Frontiers in Microbiology](https://www.frontiersin.org/journals/microbiology/articles/10.3389/fmicb.2023.1122691/full)
2. [Enterobacter spp.: Update on Taxonomy, Clinical Aspects, and Emerging Antimicrobial Resistance, PMC](https://pmc.ncbi.nlm.nih.gov/articles/PMC6750132/)
3. [Genomic Diversity within the Enterobacter cloacae Complex, PMC](https://pmc.ncbi.nlm.nih.gov/articles/PMC2515634/)
4. [Enterobacter cloacae Complex: Clinical Impact and Emerging Antibiotic Resistance, Future Microbiology](https://www.tandfonline.com/doi/full/10.2217/fmb.12.61)
5. [Mechanisms of resistance in Enterobacteriaceae towards beta-lactamase antibiotics, Acta Med Croatica (PubMed)](https://pubmed.ncbi.nlm.nih.gov/15700687/)
6. [Epidemiology and Mechanisms of Resistance of Extensively Drug Resistant Gram-Negative Bacteria, PMC](https://pmc.ncbi.nlm.nih.gov/articles/PMC6628318/)
7. [Inherent colistin resistance in genogroups of the Enterobacter cloacae complex, Journal of Antimicrobial Chemotherapy](https://academic.oup.com/jac/article/75/9/2452/5854852)
8. [Enterobacter spp.: Update on Taxonomy, Clinical Aspects, and Emerging Antimicrobial Resistance, Clinical Microbiology Reviews](https://journals.asm.org/doi/10.1128/CMR.00002-19)
9. [Revisiting Species Identification within the Enterobacter cloacae Complex by MALDI-TOF Mass Spectrometry, Microbiology Spectrum](https://doi.org/10.1128/Spectrum.00661-21)
10. [Molecular Mechanisms, Epidemiology, and Clinical Importance of β-Lactam Resistance in Enterobacteriaceae, IJMS](https://www.mdpi.com/1422-0067/21/14/5090)
11. [A Primer on AmpC β-Lactamases: Necessary Knowledge for an Increasingly Multidrug-resistant World, PubMed](https://pubmed.ncbi.nlm.nih.gov/30838380/)
12. [Emerging Transcriptional and Genomic Mechanisms Mediating Carbapenem and Polymyxin Resistance in Enterobacteriaceae, PMC](https://pmc.ncbi.nlm.nih.gov/articles/PMC7771540/)
13. [Adaptive and Mutational Resistance: Role of Porins and Efflux Pumps in Drug Resistance, PMC](https://pmc.ncbi.nlm.nih.gov/articles/PMC3485749/)
14. [A New Challenge of Antibiotic-Resistant Bacteria: Carbapenem-Resistant Enterobacter cloacae Complex in a One Health Perspective, Microorganisms](https://www.mdpi.com/2076-2607/14/3/594)
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*Topic: Encyclopedia › Life and health › Microorganisms and fungi › Bacteria › Medically important pathogenic bacteria*
*Initially written Sep 17, 2026 · Reviewed: Sep 30, 2026; Oct 21, 2026 · Edited: Sep 30, 2026; Oct 21, 2026 · Last review: Oct 21, 2026*
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License: Edgepedia Community License 1.0, https://www.edgepedia.org/edgepedia/license