Difference between revisions of "Enterobacter cloacae"

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A Microbial Biorealm page on the genus Enterobacter cloacae


Higher order taxa

Bacteria, Proteobacteria, Gammaproteobacteria, Enterobacteriales, Enterobacteriaceae, Enterobacter, Enterobacter cloacae complex, Enterobacter cloacae


NCBI: Taxonomy

Genus: Enterobacter

Species: cloacae

Description and significance

Enterobacter cloacae is a rod-shaped, gram-negative bacteria from the Enterobacteriaceae family. The size of this bacteria ranges from 0.3-0.6 x 0.8-2.0 μm. (13). Enterobacter cloacae lives in the mesophilic environment with its optimal temperature at 37 °C and uses its peritrichous flagella for movement. This organism is oxidase negative but catalase positive and is facultative anaerobic (13). In other words, this organism can make ATP by aerobic respiration when oxygen is present but can switch to fermentation in the absence of oxygen.

Enterobacter cloacae infections have the highest mortality rate compared to other Enterobacter infections. Many of the clinical samples of the Enterobacter infections are hard to distinguish from other bacterial infections, so having its genome sequenced would be very useful for treating these infections. (4)

Enterobacter cloacae are nosocomial pathogens that can cause a range of infections such as bacteremia, lower respiratory tract infection, skin and soft tissue infections, urinary tract infections, endocarditis, intra-abdominal infections, septic arthritis, osteomyelitis, and ophthalmic infections (4). This organism affects mostly the vulnerable age groups such as the elderly and the young and can cause prolonged hospitalization in the intensive care unit (ICU) (5). ICU pathogens can cause morbidity and mortality and the management of this bacteria infection is complicated by the organism’s multiple antibody resistance. These bacteria contain beta-lactamase, which is undetectable in vitro and is highly resistant to antibiotics such as third generation cephalosporins. (4)

This organism is mainly isolated as nosocomial infections in the ICU for those who stay in the hospital for prolonged periods. The infection may be contracted through the skin, gastrointestinal tract, urinary tract, or cross-contamination. Outbreaks can also be traced back to hands of personnel, endoscopes, blood products, total parenternal nutrition solutions, albumin, and hospital equipment such as stethoscopes and dialysis. (4)

Genome structure

The genomes of several strains of Enterobacter cloacae have been partially sequenced with the 16S ribosomal RNA gene. Unfortunately there are no genomes of Enterobacter cloacae that have been fully sequenced. This organism produces chromosomally encoded Beta-lactamases also called cephalosporinases. Many of the Enterobacter species have multiple antibiotic resistance that are undetectable in vitro, which makes it difficult to treat in patients (17). Some are resistant to fluoroquinoles (1).

Partial sequences for the AcrR and complete sequence of the AcrA and AcrB genes of Enterobacter cloacae are available. The AcrR gene acts as a repressor while the AcrA gene is a membrane fusion protein for the multidrug efflux pump. The AcrB gene is the inner membrane transporter for the multidrug efflux pump.

Cell structure and metabolism

Enterobacter cloacae are gram-negative bacteria which means they contain two cell walls. On the outer membrane, the lipid-A from the lipopolysaccharide (also known as endotoxins), causes sepsis. Lipid-A releases cytokines, which can cause toxins to run in the tissues and blood stream. They contain beta-lactamase, which is component that is responsible for antibiotic resistance during treatment and cannot be detected in vitro. This organism is a glucose fermenter and is able to grow in aerobic and anaerobic atmospheres. Enterobacter cloacae is positive for beta-galactosidase, arginine dihydrolase, ornithine ecarboxylase, citrate utilization, nitrate reduction, and Voges-Proskauer reaction. Although acid is produced from many carbon sources, this bacteria does not produce lysine decarboxylase, hydrogen sulfide, urease, tryptophan deaminase, and indole. (5)

Under anaerobic conditions, Enterobacter cloacae is capable of reducing selenite to elemental selenium in order to maintain its cells. In order to do o, it require menaquinone, which acts as an electron carrier. By reducing selenite with menaquinone, a proton motive force is generated, allowing the cell to slowly grow in anerobic conditions and sustain the cells(21). When glucose is used at an electron donor, it removed 79% of SeO (20). Water becomes contaminated with selenite discharges from industrial practiced such as fossil fuel combustion, petroleum refining, and mining. Senenite is soluble, toxic and and can bioaccumulate in the food chain, but Enterobacter cloacae reduces it to elemental selenium which is nontoxic and insoluble. High levels of SeO in water has been identified as the cause of embryonic deformities and the death of aquatic birds(20).


Enterobacter cloacae can be found on human skin and tissues as well as fruits, vegetables, and devices such as a hot water treatment tank. Although this organism is mainly a pathogen for human and causes disease, Enterobacter cloacae have been used as a biological control for plant disease such as the seed-rotting oomycete in Pythium ultimum and used to control insect pests on mulberry leaves and suppress disease (3).


Enterobacter cloacae are nosocomial pathogens that can be acquired through the skin, gastrointestinal tract, urinary tract or derived externally due to the ubiquitous nature. This organisms is an opportunistic pathogen, which means that the disease targets compromised patients such as the young, old, or those that have a severe disease such as human immunodeficiency virus (5). Nosocomial infections are most frequent from this organism, which means it may be contracted from the result of being hospitalized, such as the ICU. Enterobacter cloacae have been isolated from hands of personnel, endoscopes, blood products, devices for intra-arterial pressure, stethoscopes, albumim, digital thermometers and many more (4).

There have been incidences of cross-contamination in the cardiovascular ward through the transoesophageal echocardiography probe in the ICU as well as the blood culturing system. With many possibilities for outbreaks due to Enterobacter cloacae, it is important to have routine environment cleaning, especially when new methods, equipments, or personnel are introduced (8).

Enterobacter cloacae are responsible for various infections such as bacteremia, lower respiratory tract infections, skin and soft tissue infections, urinary tract infections, endocarditis, intra-abdominal infections, septic arthritis, osteomyelitis, and ophthalmic infections. These infections can cause morbidity and mortality and the infection is hard to manage due to their multiple antibiotic resistance.

Current Research

One recent study found that RamA and AcrAB genes are associated with the decreased susceptibility to tigecycline in Enterobacter cloacae. Tigecycline is an antibiotic that is used against gram-positive and gram-negative bacterial pathogens including many strains of Enterobacter cloacae. Recently, few strains of Enterobacter cloacae have been found that have decreased susceptibility to tigecycline. By using the Northern blot analysis, a mutant of E. cloacae, G946 and several other strains that have a decreased susceptibility to tigecycline showed an increased level of acrAB transcript. The results from this study show that the RamA-mediated over expression of the AcrAB efflux pump allow the decreased susceptibility to tigecycline. Research on other genes in Enterobacter cloacae can provide further knowledge about the antibiotic resistance this organism can obtain. (9)

Another recent study found that after routine surveillance in a cardiovascular ward, there was an increase of Enterobacter cloacae isolates from the sputum and oropharyngeal cultures from 5.5% to 27.6%. The data suggests cross-contamination through the transoesophageal echocardiography (TOE) probe in the ICU and was verified by using the pulsed-field gel electrophoresis and antibiogram patterns. The TOE was disinfected with a 0.55% phtharal solution and using single use sheath for the probe from getting contaminated once more. This study reveals that there needs to be improved methods in increasing the sensitivity of these outbreaks. (8)

Another recent research study investigated the chromate resistant mechanism of Enterobacter cloacae through atomic force microscopy. The strain CYS-25 of E. cloacae was isolated that showed a strong resistant to chromate in aerobic conditions. This study was done using atomic force microscopy which is used to see the morphological characteristics of the bacteria. It was shown that the length of the bacteria increased from 2.3 +/- 0.6 microm to 3.2 +/- 0.7 microm after the stimulation of 400 mg/L of chromate. This mechanism of Enterobacter cloacae is used as a survival strategy by preventing chromate into the cells.(19)

Another study showed that mutation in the cyaA gene, which encodes for adenylate cyclase in E. cloacae produced a decrease in cucumber root colonization. The strains revealed that E. cloacae can be used as a biological control agent for Pythium ultimum. The study shows that mutants and strains off E. cloacae can be used for colonization of cucumber root and perhaps used as biological control agents for other crops. (16)

Another research study was done on Enterobacter cloacae and their ability to produce beta-lactamase, also known as cephalosporinases. A new chromosomal AmpC beta-lactamase was isolated from a blood culture and revealed its resistance to aminopenicillins, aztreonam, and broad-spectrum cephalosporins. By using polymerase chain reaction (PCR), the ampC gene was amplified and cloned into the pBK-CMV vector. Sequencing revealed that 382 amino acids have an 86% identity with AmpC E. cloacae P99 and 98% identity with plasmid-borne MIR-1 beta-lactamase gene product. The data revealed that the chromosomal location of this gene is closely related to the plasmid-borne MIR-1 from Klebsiella pneumoniae. (17)

Another research study recently done was on the antibiotic resistance of Enterobacter cloacae that was isolated from food animals such as ground beef cattle farm, processing facilities and clinical settings. The ampC, ampD and ampR genes were sequenced and analyzed. The ampC gene was cloned into E. coli strains and analyzed through pulse field gel electrophoresis. AmpR were resistant to beta-lactam agents and ampC showed resistance to ampicillin, cephalothin and amoxicillin. The experiment data suggests that AmpC producing Enterobacter cloacae could be a contributor in spreading the beta-lactamase genes in the farm and food processing environments. (10)

Studies have shown that Enterobacter cloacae has caused an outbreak of infections in many hospital burn centers. It was noted that the development of this bacteria was related to the severity of third degree burns and admission into these burn centers. Researchers have found that E. cloacae is a common inhabitant of hospital equipment such as IV’s (22). According to a journal written by Joseph, Sharbaugh, and Bannister, it was found that the second outbreak of isolated Enterobacter cloacae were resistant to tobramycin, amikacin, and silver nitrate. In addition, it was found that the plasmid content in these strains were different from the bacteria in the first outbreak (23). As a result, discovering a therapy to fight off infections caused by this bacteria is very complicated due to the multiresistant strains of E. cloacae. The most effective agent against this bacteria is aminoglycosides, yet more drugs are becoming available to target the infection caused by Enterobacter cloacae. Antibiotics such as cefotaxime and cefaperazone are currently in use and may be used as one of the primary drugs to fight off infections caused by these bacteria (23).


(1) Davin-Regli A, Bosi C, Charrel R, Ageron E, Papazian L, Grimont P, Cremieux A, Bollet C. “A Nosocomial Outbreak Due to Enterobacter cloacae Strains with the E. hormaechei Genotype in Patients Treated with Fluoroquinolones.” Journal of Clinical Microbiology. Vol. 35, No. 4. Apr. 1997: p. 1008-1010.

(2) Deal EN, Micek ST, Ritchie DJ, Reichley RM, Dunne WM Jr, Kollef MH. “Predictors of in-hospital mortality for bloodstream infections caused by Enterobacter species or Citrobacter freundii.” Feb 2007; 27(2):191-9. http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17253909&ordinalpos=62&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

(3) Dijk, Karin van, Nelson, Eric B. “Fatty Acid Competition as a Mechanism by which Enterobacter cloacae Suppresses Pythium ultimum Sporangium Germination and Damping-Off.” Applied and Environmental Microbiology. Vol. 66, No. 12. Dec 2000. p. 5340-5347. http://aem.asm.org/cgi/content/abstract/66/12/5340

(4) Fraser, Susan L. “Enterobacter Infections.” eMedicine. 8 Jan 2007. http://www.emedicine.com/med/topic678.htm

(5) Hopley, Lara, Schalkwyk, Jo van. “Enterobacter.” 29 Sept 2001. http://www.anaesthetist.com/icu/infect/bacteria/gramneg/Findex.htm#enterobacter.htm

(6) Ibenyassine K, Mhand RA, Karamoko Y, Anajjar B, Chouibani MM, Ennaji M. “Bacterial pathogens recovered from vegetables irrigated by wastewater in Morocco.” PubMed. Jun 2007; 69(10):47-51. http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17583296&ordinalpos=18&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

(7) Juanjuan D, Zhiyong Z, Xiaoju L, Yali X, Xihai Z, Zhenzhen L. “Retrospective analysis of bacteremia because of Enterobacter cloacae compared with Escherichia coli bacteremia.” April 2007; 61(4):583-8. http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17394432&ordinalpos=40&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

(8) Kanemitsu K, Endo S, Oda K, Saito K, Kunishima H, Hatta M, Inden K, Kaku M. “An increased incidence of Enterobacter cloacae in a cardiovascular ward.” Jun 2007; 66(2):130-4. http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17512633&ordinalpos=29&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

(9) Keeney D, Ruzin A, Bradford PA. “RamA, a transcriptional regulator, and AcrAB, an RND-type efflux pump, are associated with decreased susceptibility to tigecycline in Enterobacter cloacae.” 2007 Spring; 13(1):1-6. http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17536927&ordinalpos=27&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

(10) Kim SH, Wei CI. “Expression of AmpC beta-lactamase in Enterobacter cloacae isolated from retail ground beef, cattle farm and processing facilities.” Aug 2007:103(2):400-8. http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17650200&ordinalpos=10&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

(11) Mahapatra A, Ghosh SK, Mishra S, Pattnaik D, Pattnaik K, Mohanty SK. Enterobacter cloacae: A predominant pathogen in neonatal septicaemia. Indian J Med Microbiol 2002;20:110-112.

(12) Manzur A, Tubau F, Pujol M, Calatayud L, Dominguez MA, et al. “Nosocomial Outbreak Due to Extended-Spectrum-Beta-Lactamase- Producing Enterobacter cloacae in a Cardiothoracic Intensive Care Unit.” April-Jun 2002; 20(2):110-2. http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17657046&ordinalpos=7&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

(13) Nishijima, K.A. “Enterobacter cloacae.” Crop Knowledge Master. Jan 1999. http://www.extento.hawaii.edu/Kbase/crop/Type/e_cloac.htm

(14) Pearson M L, Pegues D A, Carson L A, O’Donnell R, Berger R H, Anderson R L, Jarvis W R. “Cluster of Enterobacter cloacae pseudobacteremias associated with use of an agar slant blood culturing system.” Oct 1993; 31(10): 2599-2603. http://www.pubmed.nih.gov/articlerender.fcgi?artid=265943

(15) Roberts, Daniel P. USDA Agricultural Research Service. 20 Feb 2007. http://www.ars.usda.gov/pandp/people/people.htm?personid=4747&pf=1

(16) Roberts DP, McKenna LF, Hu X, Lohrke SM, Kong HS, de Souza JT, Baker CJ, Lydon J. “Mutation in cyaA in Enterobacter cloacae decreases cucumber root colonization.” Feb 2007; 187(2):101-15. http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17024489&ordinalpos=84&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

(17) T. Conceicao, N. Faria, M. Pimentel, G. Soveral, A. Duarte, et al. “New Chromosomal AmpC ß-Lactamase in Enterobacter cloacae.” PubMed Central. April 2004. http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=375280

(18) Yamamoto A, Konishi E, Kumata M. “[Drug-resistant bacteria isolated from pharyngeal swab cultures and urine in acutely or chronically febrile elderly nursing home inmates].” May 2007;44(3):331-8. http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17575437&ordinalpos=21&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

(19) Yang C, Cheng Y, Ma X, Zhu Y, Holman HY, Lin Z, Wang C. “Surface-mediated chromate-resistant mechanism of Enterobacter cloacae bacteria investigated by atomic force microscopy.” 10 April 2007; 23(8):4480-5. http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17371056&ordinalpos=42&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

(20) Dungan, R.S., and W.T. Frankenberger. "Reduction of Selenite to Elemental Selenium by Enterobacter Cloacae SLD1a-1." Journal of Environmental Quality ,1998. Volume 27. p.1301-306. <http://vnweb.hwwilsonweb.com/hww/results/results_single.jhtml;hwwilsonid=0FP2OQ3YYEUSBQA3DIKSFGOADUNGIIV0>.

(21) Jincai M, Donald Y. Kobayashi, and Nathan Yee. “Role of Menaquinone Biosynthesis Genes in Selenate Reduction by Enterobacter cloacae SLD1a-1 and Eschericia coli K12.” Environmental Microbiology, 2009. Vol 11, No. 1. p. 149-158. <http://web.ebscohost.com/ehost/pdfviewer/pdfviewer?vid=7&hid=14&sid=e9d0649b-a58d-44bb-95b4-bec0379836eb%40sessionmgr10>.

(22) C. Glen Mayhall, V. Archer Lamb, William E. Gayle Jr. and Boyd W. Haynes Jr. “Enterobacter cloacae Septicemia in a Burn Center: Epidemiology and Control of an Outbreak.” The Journal of Infectious Diseases. Vol. 139, No. 2 (Feb., 1979), pp. 166-171. <http://www.jstor.org/stable/30110499 >

(23) Joseph F. John, Jr., Robert J. Sharbaugh and Edward R. Bannister. “Enterobacter cloacae: Bacteremia, Epidemiology, and Antibiotic Resistance.” Reviews of Infectious Diseases. Vol. 4, No. 1 (Jan. - Feb., 1982), pp. 13-28. <http://www.jstor.org/pss/4452695>

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