eMedicine Specialties > Infectious Diseases > Bacterial Infections

Enterobacter Infections: Treatment & Medication

Author: Susan L Fraser, MD, Infectious Diseases Service, Walter Reed Army Medical Center; Chairman, Infection Control Committee; Associate Professor of Medicine, Uniformed Services University of the Health Sciences
Coauthor(s): Michael Arnett, MD, Resident, Department of Medicine, Tripler Army Medical Center; Christian P Sinave, MD, Associate Professor, Department of Medical Microbiology and Infectious Diseases, University of Sherbrooke, Canada
Contributor Information and Disclosures

Updated: Aug 28, 2008

Treatment

Medical Care

Antimicrobial therapy is indicated in virtually all Enterobacter infections.

With few exceptions, the major classes of antibiotics used to manage infections with these bacteria include the beta-lactams, the fluoroquinolones, the aminoglycosides, and TMP-SMZ. Because most Enterobacter species are either very resistant to these agents or can develop resistance during antimicrobial therapy, the choice of appropriate antimicrobial agents is complicated. Consultation with experts in infectious diseases and microbiology is usually indicated. In 2006, Paterson published a good review of resistance among various Enterobacteriaceae.16

Newer options include tigecycline. Although not indicated specifically for Enterobacter pneumonia or bloodstream infections, tigecycline has excellent in vitro activity against these gram-negative bacilli.17,18,19 In one laboratory study of multidrug-resistant gram-negative bacilli, tigecycline maintained a low MIC against all of the organisms.20 Older options might include intravenous administration of polymyxin B or colistin, drugs that are rarely used, even in large medical centers, and for which standard susceptibility criteria are not available.

  • Beta-lactams
    • With rare exceptions, E cloacae, E aerogenes, and most other Enterobacter species are resistant to the narrow-spectrum penicillins that traditionally have good activity against other Enterobacteriaceae such as E coli (eg, ampicillin, amoxicillin) and to first-generation and second-generation cephalosporins (eg, cefazolin, cefuroxime). They also are usually resistant to cephamycins such as cefoxitin. Initial resistance to third-generation cephalosporins (eg, ceftriaxone, cefotaxime, ceftazidime) and extended-spectrum penicillins (eg, ticarcillin, azlocillin, piperacillin) varies but can develop during treatment. The activity of the fourth-generation cephalosporins (eg, cefepime) is fair, and the activity of the carbapenems (eg, imipenem, meropenem, ertapenem, doripenem) is excellent. However, resistance has been reported, even to these agents.
    • The bacteria designated by the acronym SERMOR-PROVENF (SER = Serratia, MOR = Morganella, PROV = Providencia, EN = Enterobacter, F = freundii for Citrobacter freundii) have similar, although not identical, chromosomal beta-lactamase genes that are inducible. With Enterobacter, the expression of the gene AmpC is repressed, but derepression can be induced by beta-lactams. Of these inducible bacteria, mutants with constitutive hyperproduction of beta-lactamases can emerge at a rate between 105 and 108. These mutants are highly resistant to most beta-lactam antibiotics and are considered stably derepressed.
    • AmpC beta-lactamases are from the functional group 1 and molecular class C in the Bush-Jacoby-Medeiros classification of beta-lactamases. They are not inhibited by beta-lactamase inhibitors (eg, clavulanic acid, tazobactam, sulbactam). Ampicillin and amoxicillin, first- and second-generation cephalosporins, and cephamycins are strong AmpC beta-lactamase inducers. They are also rapidly inactivated by these beta-lactamases; thus, resistance is readily documented in vitro.
    • Third-generation cephalosporins and extended-spectrum penicillins, although labile to AmpC beta-lactamases, are weak inducers. Resistance is expressed in vitro only with bacteria that are in a state of stable derepression (mutant hyperproducers of beta-lactamases). However, the physician must understand that organisms considered susceptible with in vitro testing can become resistant during treatment by the following sequence of events: (1) induction of AmpC beta-lactamases, (2) mutation among induced strains, (3) hyperproduction of AmpC beta-lactamases by mutants (stable derepression), and (4) selection of the resistant mutants (the wild type sensitive organisms being killed by the antibiotic).
    • For unknown reasons, extended-spectrum penicillins are less selective than third-generation cephalosporins. The in-therapy resistance phenomenon is less common with carboxy, ureido, or acylaminopenicillins. This phenomenon has been well documented as a cause of treatment failure with pneumonia and bacteremia; however, the phenomenon is rare with UTIs.
    • Carbapenems are strong AmpC beta-lactamase inducers, but they remain very stable to the action of these beta-lactamases. As a consequence, no resistance to carbapenems, either in vitro or in vivo, can be attributed to AmpC beta-lactamases.
    • The fourth-generation cephalosporins are relatively stable to the action of these beta-lactamases; consequently, they retain moderate activity against the mutant strains of Enterobacter, hyperproducing AmpC beta-lactamases.
    • More recently, the production of extended-spectrum beta-lactamases (ESBLs) has been documented in Enterobacter. Usually, these ESBLs are TEM1 -derived or SHV1 -derived enzymes, and they have been reported since 1983 in Klebsiella pneumoniae, Klebsiella oxytoca, and E coli. Bush et al classify these ESBLs in group 2be and in molecular class A in their beta-lactamase classification.21 The location of these enzymes on plasmids favors their transfer between bacteria of the same and of different genera. Many other gram-negative bacilli may also possess such resistant plasmids.
    • Among Enterobacter species, reports indicate that E aerogenes has been the most common carrier of ESBL. Unlike the AmpC beta-lactamases, these enzymes are encoded by plasmid DNA and do not possess a molecular mechanism of induction or stable derepression. They are inactivated by the beta-lactamase inhibitors and remain susceptible to cefoxitin (testing cefoxitin is then a useful tool to help differentiate AmpC beta-lactamases from ESBLs).
    • Bacteria-producing ESBLs should be considered resistant to all generations of cephalosporins, all penicillins, and to the monobactams such as aztreonam, even if the in vitro susceptibilities are in the sensitive range according to the CLSI breakpoints. In the past, the CLSI has cautioned physicians regarding the absence of a good correlation with susceptibility when its breakpoints are applied to ESBL-producing bacteria.
    • In 1999, this committee published guidelines for presumptive identification and for confirmation of ESBL production by Klebsiella and E coli, guidelines that are often applied to other Enterobacteriaceae. From the above, one can conclude that, when a bacterium of the genus Enterobacter produces ESBL(s) (more than 1 ESBL can be produced by the same bacteria), it does so in addition to the AmpC beta-lactamases that are always present, either in states of inducibility or in states of stable derepression. With stable derepressed mutants, ESBL is almost impossible to detect unless molecular methods such as polymerase chain reaction (PCR) or isoelectric focusing (IEF) electrophoresis are used. For inducible strains, no recommendations have been issued by the CLSI for the detection of ESBL (ie, if PCR and IEF electrophoresis are not readily available).
    • Carbapenems are the only reliable beta-lactam drugs for the treatment of severe Enterobacter infections, and fourth-generation cephalosporins are a distant second choice. The association of an extended-spectrum penicillin with a beta-lactamase inhibitor remains a controversial issue for therapy of ESBL-producing organisms.
    • Resistance to carbapenems is rare but has been reported and is considered an emerging clinical threat posed by Enterobacter species, as well as by other Enterobacteriaceae. The beta-lactamases first implicated in imipenem resistance were NMC-A and IMI-1, both molecular class A and functional group 2f carbapenemases, which are inhibited by clavulanic acid and then able to hydrolyze all the beta-lactams not associated with a beta-lactamase inhibitor.
    • Hyperproduction (stable derepression) of AmpC beta-lactamases associated with some decrease in permeability to the carbapenems may also cause resistance to these agents. In vitro low-level ertapenem resistance was not associated with resistance to imipenem or meropenem, but high-level ertapenem resistance predicted resistance to the other carbapenems.22
    • Metallo-beta-lactamases cause resistance across the carbapenem class, are transmissible, and have been associated with clinical outbreaks in hospitals worldwide. In one reported outbreak of 17 cases of infection (2 due to Enterobacter species), molecular studies demonstrated presence of a gene belonging to bla(VIM-1) cluster.23 KPC-type carbapenemases have emerged in New York City.16
  • Aminoglycosides
    • Aminoglycoside resistance is relatively common and varies widely among centers.
    • As with other members of Enterobacteriaceae, this resistance results from the production of different aminoglycoside-inactivating enzymes.
  • Quinolones and TMP-SMZ
    • Resistance to fluoroquinolones is relatively rare but may be high in some parts of the world.
    • Resistance to TMP-SMZ is more common.
  • Colistin and polymyxin B: These drugs are being used more frequently to treat serious infection caused by multidrug-resistant organisms, sometimes as monotherapy or in combination with other antibiotics. Clinical experience, including documentation of success rates and attributable mortality is broadening.24 Heteroresistance to colistin was demonstrated in a few Enterobacter isolates collected from ICU patients and was best identified using broth microdilution, agar dilution, or E-test methods.25 Polymyxin B was not as active against Enterobacter species as it was against other Enterobacteriaceae but did demonstrate an MIC50 of less than or equal to 1, with 83% of Enterobacter isolates considered susceptible.26

Surgical Care

Surgical care is indicated as for other sources of infection: drainage or debridement of abscesses, infected collections, or osteomyelitic foci.

In some instances, the clinician must consider this option instead of percutaneous drainage with CT guidance. The severity of the infection and the size of the collection to be drained are among the parameters to consider when choosing the best option for the patient.

For endocarditis, valvular replacement is also indicated, particularly in patients with emboli or intractable heart failure.

Consultations

Enterobacter species cause severe and frequently life-threatening infections that can originate in virtually any body compartment. Enterobacter infection warrants consultation with many different subspecialists.

  • Consultation with an infectious diseases specialist helps in the selection of antimicrobial agents, taking into account the multiple mechanisms of resistance to different classes of antimicrobial agents and the lack of correlation between crude in vitro susceptibility results and true clinical efficacy for most of the beta-lactams.
  • Intensive care specialists, when appropriate, can help in the management of severe sepsis or septic shock.
  • General internal medicine and/or medical subspecialists (eg, cardiologists, gastroenterologists, nephrologists, rheumatologists, pulmonologists) may be helpful.
  • Surgeons may help with the drainage of infected collections, if indicated, as well as with debridement of necrotic tissues.
  • Consult neonatologists for neonatal sepsis and, possibly, general pediatricians or pediatric subspecialists (including pediatric surgeons).
  • Radiologists and nuclear medicine physicians may help select the best imaging study according to patient's specific problems and (radiologists) may be needed to perform percutaneous drainage of infected collections.
  • A microbiologist can provide valuable assistance by educating clinicians regarding the correct interpretation of susceptibility testing with this organism.

Medication

The goals of pharmacotherapy are to eradicate the infection, to reduce morbidity, and to prevent complications.

Antibiotics

The antimicrobials most indicated in Enterobacter infections include carbapenems, fourth-generation cephalosporins, aminoglycosides, fluoroquinolones, and TMP-SMZ.

Carbapenems have the best activity against E cloacae, E aerogenes, and others. They are not affected by ESBLs. Imipenem-cilastatin and meropenem are used most often. Ertapenem, approved more recently, is gaining clinical experience.27 Doripenem, recently approved in the United States, is likely to be as effective.

First-generation and second-generation cephalosporins are inactive against Enterobacter infections. Third-generation cephalosporins frequently show good in vitro activity against these organisms, but, as explained above, a significant risk of developing full resistance during therapy exists. Resistance develops much less frequently with fourth-generation cephalosporins because they are relatively stable to AmpC beta-lactamase but not (so far) to the less frequently encountered ESBLs (see Medical Care). Third-generation cephalosporins are not indicated for the treatment of severe Enterobacter infections, perhaps with the notable exception of uncomplicated infections.

Fluoroquinolones have good bactericidal activity against gram-negative bacilli; their bioavailability ranges from very good to excellent (with the exception of norfloxacin). Newer quinolones have increased their spectrum toward gram-positive organisms and, in some cases, toward anaerobes. Ciprofloxacin and levofloxacin have the best activity against gram-negative bacilli and should generally be selected over the newer fluoroquinolones if clinically indicated.


Polymyxin B

Binds to phospholipids, alters permeability, and damages bacterial cytoplasmic membrane.

Adult

15,000-25,000 U/kg/d IV divided q12h

Pediatric

<2 years: Not established
>2 years: Administer as in adults

May increase or prolong effect of neuromuscular blocking agents

Documented hypersensitivity to drug or components of formulation; concurrent use of neuromuscular blockers

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Prolonged use of antibiotics or repeated therapy may result in bacterial or fungal overgrowth of nonsusceptible organisms


Levofloxacin (Levaquin)

In addition to ciprofloxacin, levofloxacin is an alternative choice. It has the advantage of once daily dosing, whether administered IV or PO.
Used for pseudomonal infections and infections due to multidrug-resistant gram-negative organisms.

Adult

500-750 mg PO/IV qd

Pediatric

<18 years: Not recommended
>18 years: Administer as in adults

Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; levofloxacin reduces therapeutic effects of phenytoin; probenecid may increase levofloxacin serum concentrations

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy


Doripenem (Doribax)

Carbapenem antibiotic. Doripenem is a new alternative choice. Has spectrum of activity similar to that of imipenem and meropenem (Fritsche, 2005; Mushtaq, 2004).
Elicits activity against a wide range of gram-positive and gram-negative bacteria. Indicated as a single agent for complicated intra-abdominal infections caused by susceptible strains of E coli, K pneumoniae, P aeruginosa, Bacteroides caccae, Bacteroides fragilis, Bacteroides thetaiotaomicron, Bacteroides uniformis, Bacteroides vulgatus, Streptococcus intermedius, Streptococcus constellatus, and Peptostreptococcus micros.

Adult

500 mg IV q8h infused over 1 h
CrCl 30-49: 250 mg IV q8h
CrCl 11-29: 250 mg IV q12h

Pediatric

<18 years: Not established
>18 years: Administer as in adults

Carbapenems may decrease valproic acid serum concentration, causing increased seizure risk; probenecid reduces renal clearance of doripenem, resulting in increased doripenem concentration; does not inhibit or induce major CYP450 enzymes

Documented hypersensitivity to doripenem or other carbapenems or demonstrated anaphylactic reactions to beta-lactams

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Clostridium difficile –associated diarrhea has been reported with nearly all antibacterial agents and must be considered in patients with diarrhea; common adverse effects (ie, >5%) include headache, nausea, diarrhea, rash, and phlebitis; decrease dose with renal insufficiency


Imipenem/cilastatin (Primaxin)

For treatment of multiple-organism infections in which other agents do not have wide-spectrum coverage or are contraindicated because of potential toxicity. DOC for severe Enterobacter infections, except for meningitis and other CNS infections because of some reports indicating higher seizure potential. Hydrolyzed by the renal dehydropeptidase-1. To overcome this urinary inactivation, cilastatin, an inhibitor of this renal enzyme, is administered in equal amounts.

Adult

500-1000 mg IV q6h; majority of severe infections can be treated with 2 g/d

Pediatric

Age <1 week: 25 mg/kg IV q12h
Age 1-4 weeks: 25 mg/kg IV q8h
Age 4 weeks to 3 months: 25 mg/kg IV q6h
15-25 mg/kg/dose IV q6h suggested for >3 mo
Imipenem should not be used in pediatric CNS infections or in infants with impaired renal function who weigh <30 kg
Fully susceptible organisms: Not to exceed 2 g/d
Moderately susceptible organisms: Not to exceed 4 g/d

Coadministration with cyclosporine may increase adverse CNS effects of both agents; coadministration with ganciclovir may result in generalized seizures

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Adjust dose in renal insufficiency (adult adjustments)
CrCl (mL/min) 80-50: 0.5 g IV q6-8h
CrCl 50-10: 0.5 g IV q8-12h
Hemodialysis (HD): 0.25-0.5 g after HD, then q12h
Higher doses significantly increase risk of seizures


Meropenem (Merrem IV)

Alternative to imipenem for severe Enterobacter infections. Carbapenem of choice for meningitis and for patients at risk for seizures. Bactericidal broad-spectrum carbapenem antibiotic that inhibits cell wall synthesis. Effective against most gram-positive and gram-negative bacteria. Not degraded by renal dehydropeptidase-1. Has slightly increased activity against gram-negative organisms and slightly decreased activity against staphylococci and streptococci compared to imipenem.

Adult

0.5-2 g IV q8-12h

Pediatric

20-40 mg/kg IV q8h

Probenecid may inhibit renal excretion, thereby increasing levels

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Dosage adjustments (adult adjustments)
CrCl (mL/min) 50-10: 0.5-1 g IV q12h
CrCl <10: 0.5 g/d IV
HD: As for CrCl <10, with an extra 0.5 g after HD
Pseudomembranous colitis and thrombocytopenia may occur, requiring immediate discontinuation of medication


Cefepime (Maxipime)

Fourth-generation cephalosporin with good gram-negative coverage. Similar to third-generation cephalosporins but has better gram-positive coverage.

Adult

0.5-2 g IV q8-12h

Pediatric

50 mg/kg IV q8-12h; not to exceed 2 g

High dose decreases clearance; when used concurrently, aminoglycosides, furosemide, ethacrynic acid, and vancomycin increase nephrotoxic potential

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Dosage adjustments (adult adjustments)
CrCl (mL/min) 80-50: 0.5-2 g IV q12-24h
CrCl 50-10: 0.5-2 g/d IV
CrCl <10: 0.25-0.5 g/d IV
HD: as for CrCl <10, with an extra 0.25 g after HD
During peritoneal dialysis: 1-2 g IV q48h
Prolonged use may predispose patients to superinfection


Ciprofloxacin (Cipro)

Fluoroquinolone with good activity against pseudomonads and most gram-negative organisms, but no activity against anaerobes. Inhibits bacterial DNA synthesis and, consequently, growth. Among fluoroquinolones, ciprofloxacin has the best activity against the gram-negative bacilli (including Enterobacter). IV and PO formulations available. Oral bioavailability is approximately 80%.

Adult

250-750 mg PO q12h; alternatively, 200-400 mg IV q8-12h

Pediatric

25 mg/kg/d PO divided doses q12h; alternatively, 3.2-12.5 mg/kg/d IV divided doses q12h
Usually contraindicated in children before puberty unless benefits outweigh risks; limited experience, particularly in children with cystic fibrosis, seems to indicate safety

Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; reduces therapeutic effects of phenytoin; probenecid may increase serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Dosage adjustments (adult adjustments)
CrCl (mL/min) <10: 50% of PO or IV dose q12h
HD: 0.25-0.5 g PO or 0.2-0.4 g IV q12h
During peritoneal dialysis: 0.25-0.5 g PO or 0.2-0.4 g IV q8h
In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); superinfections may occur with prolonged or repeated antibiotic therapy


Trimethoprim-sulfamethoxazole (Septra, Bactrim)

Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid. Antibacterial activity of TMP-SMZ includes common urinary tract pathogens, except P aeruginosa. Susceptibility of Enterobacter generally good but varies among centers.

Adult

160 mg TMP/800 mg SMZ PO q12-24h
Alternatively, 3-5 mg/kg IV q6-8h (based on TMP component)

Pediatric

<2 months: Do not administer
>2 months: 6-12 mg/kg/d, based on TMP, PO/IV tid/qid

May increase PT when used with warfarin (perform coagulation tests and adjust dose accordingly); coadministration with dapsone may increase blood levels of both drugs; coadministration of diuretics increases incidence of thrombocytopenia purpura in elderly patients; phenytoin levels may increase with coadministration; may potentiate effects of methotrexate in bone marrow depression; hypoglycemic response to sulfonylureas may increase with coadministration; may increase levels of zidovudine

Documented hypersensitivity; megaloblastic anemia resulting from folate deficiency

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Dosage adjustments (adult adjustments)
CrCl (mL/min) 80-50: Recommended IV dose q18h
CrCl 50-10: Recommended IV dose q24h
CrCl <10: Not recommended
HD: 4-5 mg/kg after HD
During peritoneal dialysis: 0.16-0.8 g q48h
Discontinue at first appearance of skin rash or sign of adverse reaction; obtain CBC counts frequently; discontinue therapy if significant hematologic changes occur; goiter, diuresis, and hypoglycemia may occur with sulfonamides; prolonged IV infusions or high doses may cause bone marrow depression (if signs occur, give 5-15 mg/d leucovorin); caution in folate deficiency (eg, chronic alcoholism, elderly patients, those receiving anticonvulsant therapy, or those with malabsorption syndrome); hemolysis may occur in individuals with G-6-PD deficiency; patients with AIDS may not tolerate or respond to TMP-SMZ; caution in renal or hepatic impairment (perform urinalyses and renal function tests during therapy); give fluids to prevent crystalluria and stone formation


Ertapenem (Invanz)

Bactericidal activity results from inhibition of cell wall synthesis and is mediated through ertapenem binding to penicillin-binding proteins. Stable against hydrolysis by various beta-lactamases, including penicillinases, cephalosporinases, and extended-spectrum beta-lactamases. Hydrolyzed by metallo-beta-lactamases.

Adult

1 g qd for 14 d if IV and 7 d if IM; infuse over 30 min if IV
CrCl <30 mL/min/1.73 m2: 500 mg IV qd

Pediatric

<3 months: Not established
3 months to 12 years: 15 mg/kg IV q12h; not to exceed 1 g/d
>13 years: Administer as in adults

Probenecid may reduce renal clearance of ertapenem and increase half-life but benefit is minimum and does not justify coadministration

Documented hypersensitivity to drug or amide type anesthetics

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Pseudomembranous colitis may occur; seizures and CNS adverse reactions may occur; when using with lidocaine to administer intramuscularly, avoid inadvertent injection into blood vessel; decrease dose in renal failure; serious and occasionally fatal hypersensitivity reactions may occur with beta-lactams (caution with previous hypersensitivity reactions to penicillin, cephalosporins, other beta-lactams, other allergens); do not mix or coinfuse in same IV line as other medications; do not mix with dextrose-containing diluents


Tigecycline (Tygacil)

This drug is FDA approved for complicated intra-abdominal or skin and soft-tissue infections. A glycylcycline antibiotic that is structurally similar to tetracycline antibiotics. Inhibits bacterial protein translation by binding to 30S ribosomal subunit and blocks entry of amino-acyl tRNA molecules in ribosome A site. Complicated intra-abdominal infections caused by C freundii, E cloacae, E coli, K oxytoca, K pneumoniae, E faecalis (vancomycin-susceptible isolates only), S aureus (methicillin-susceptible isolates only), S anginosus group (includes S anginosus, S intermedius, S constellatus), B fragilis, B thetaiotaomicron, B uniformis, B vulgatus, C perfringens, and P micros.

Adult

Infuse each dose over 30-60 min
100 mg IV once, then 50 mg IV q12h
Severe hepatic impairment (ie, Child Pugh class C): 100 mg IV once, then 25 mg IV q12h

Pediatric

<18 years: Not established
>18 years: Administer as in adults

Coadministration decreases warfarin clearance and increases warfarin Cmax and AUC (monitor aPTT and INR); coadministration of antibiotics with oral contraceptives may decrease contraceptive effect

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in severe hepatic impairment (reduce dose); may adversely effect tooth development; may permit clostridial overgrowth, resulting in antibiotic-associated colitis; may have adverse effects similar to tetracyclines (eg, photosensitivity, pseudotumor cerebri, pancreatitis, antianabolic action)

More on Enterobacter Infections

Overview: Enterobacter Infections
Differential Diagnoses & Workup: Enterobacter Infections
Treatment & Medication: Enterobacter Infections
Follow-up: Enterobacter Infections
Multimedia: Enterobacter Infections
References
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Further Reading

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Keywords

Enterobacter infections, Enterobacter cloacae infection, Enterobacter aerogenes infection, Enterobacter sakazakii infection, Enterobacteriaceae infections, E cloacae, E aerogenes, E sakazakii, Enterobacter bacteremia, Enterobacter lower respiratory tract infection, Enterobacter skin infection, Enterobacter soft-tissue infection, Enterobacter urinary tract infection, Enterobacter UTI, Enterobacter endocarditis, Enterobacter intra-abdominal infection, Enterobacter intraabdominal infection, Enterobacter septic arthritis, Enterobacter osteomyelitis, Enterobacter ophthalmic infections, nosocomial Enterobacter infection, Enterobacter pneumonia, Enterobacter taylorae, E taylorae, Enterobacter cancerogenus, E cancerogenus

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Contributor Information and Disclosures

Author

Susan L Fraser, MD, Infectious Diseases Service, Walter Reed Army Medical Center; Chairman, Infection Control Committee; Associate Professor of Medicine, Uniformed Services University of the Health Sciences
Susan L Fraser, MD is a member of the following medical societies: American College of Physicians, American Liver Foundation, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Armed Forces Infectious Diseases Society, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Coauthor(s)

Michael Arnett, MD, Resident, Department of Medicine, Tripler Army Medical Center
Disclosure: Nothing to disclose.

Christian P Sinave, MD, Associate Professor, Department of Medical Microbiology and Infectious Diseases, University of Sherbrooke, Canada
Christian P Sinave, MD is a member of the following medical societies: American Society for Microbiology and Canadian Infectious Disease Society
Disclosure: Nothing to disclose.

Medical Editor

Maria D Mileno, MD, Assistant Professor, Department of Internal Medicine, Division of Infectious Diseases, Brown University
Maria D Mileno, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, International Society of Travel Medicine, and Sigma Xi
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Joseph F John Jr, MD, FACP, FIDSA, FSHEA, Clinical Professor of Medicine, Molecular Genetics and Microbiology, Medical University of South Carolina; Associate Chief of Staff for Education, Ralph H Johnson Veterans Affairs Medical Center
Disclosure: BioMerieux Honoraria Review panel membership; Cubist Honoraria Review panel membership; Pfizer Honoraria Speaking and teaching; Merck Stock dividends stock holdings

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

 
 
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