Enterobacter Infections Treatment & Management

  • Author: Susan L Fraser, MD; Chief Editor: Burke A Cunha, MD   more...
 
Updated: Jan 7, 2010
 

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.[18]

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.[19, 20, 21] In one laboratory study of multidrug-resistant gram-negative bacilli, tigecycline maintained a low MIC against all of the organisms.[22] 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. Ritchie et al (2009) published a good discussion regarding antibiotic choices for infection encountered in the ICU.[23]

  • 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 cephalosporinases 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 but may emerge rapidly in vivo. Jacoby (2009) recently published a good discussion about the emerging importance of AmpC beta-lactamases.[24]
    • 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 (eg, piperacillin), 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. However, Enterobacter species can develop resistance to carbapenems via other mechanisms.
    • The fourth-generation cephalosporins are relatively stable to the action of AmpC 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.[25] 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, the CLSI 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.[26]
    • 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.[27] KPC-type carbapenemases have emerged in New York City.[18]
  • 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.[28] [29] 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.[30] 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.[31] One recent in vitro study documented a colistin MIC90 of 2 mcg/mL or less in more than 90% of Enterobacter isolates from Canada.[32]
Next

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.

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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.
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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 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.

Specialty Editor Board

Maria D Mileno, MD  Associate Professor of Medicine, Division of Infectious Diseases, Alpert Medical School of 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.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Joseph F John Jr, MD, FACP, FIDSA, FSHEA  Clinical Professor of Medicine, Molecular Genetics and Microbiology, Medical University of South Carolina College of Medicine; Associate Chief of Staff for Education, Ralph H Johnson Veterans Affairs Medical Center

Disclosure: Nothing to disclose.

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.

References

  1. Lockhart SR, Abramson MA, Beekmann SE, et al. Antimicrobial resistance among Gram-negative bacilli causing infections in intensive care unit patients in the United States between 1993 and 2004. J Clin Microbiol. Oct 2007;45(10):3352-9. [Medline].

  2. Hidron AI, Edwards JR, Patel J, Horan TC, Sievert DM, Pollock DA. NHSN annual update: antimicrobial-resistant pathogens associated with healthcare-associated infections: annual summary of data reported to the National Healthcare Safety Network at the Centers for Disease Control and Prevention, 2006-2007. Infect Control Hosp Epidemiol. Nov 2008;29(11):996-1011. [Medline].

  3. National Nosocomial Infections Surveillance System. National Nosocomial Infections Surveillance (NNIS) report, data summary from October 1986-April 1997, issued May 1997. A report from the NNIS System. Am J Infect Control. Dec 1997;25(6):477-87. [Medline].

  4. National Nosocomial Infections Surveillance System. National Nosocomial Infections Surveillance (NNIS) System report, data summary from January 1990-May 1999, issued June 1999. Am J Infect Control. Dec 1999;27(6):520-32. [Medline].

  5. National Nosocomial Infections Surveillance System. National Nosocomial Infections Surveillance (NNIS) System Report, data summary from January 1992 through June 2004, issued October 2004. Am J Infect Control. Dec 2004;32(8):470-85. [Medline].

  6. National Nosocomial Infections Surveillance System. Intensive Care Antimicrobial Resistance Epidemiology (ICARE) Surveillance Report, data summary from January 1996 through December 1997: A report from the National Nosocomial Infections Surveillance (NNIS) System. Am J Infect Control. Jun 1999;27(3):279-84. [Medline].

  7. Rossi F, Baquero F, Hsueh PR, et al. In vitro susceptibilities of aerobic and facultatively anaerobic Gram-negative bacilli isolated from patients with intra-abdominal infections worldwide: 2004 results from SMART (Study for Monitoring Antimicrobial Resistance Trends). J Antimicrob Chemother. Jul 2006;58(1):205-10. [Medline].

  8. Chow JW, Satishchandran V, Snyder TA, et al. In vitro susceptibilities of aerobic and facultative gram-negative bacilli isolated from patients with intra-abdominal infections worldwide: the 2002 Study for Monitoring Antimicrobial Resistance Trends (SMART). Surg Infect (Larchmt). Winter 2005;6(4):439-48. [Medline].

  9. Deal EN, Micek ST, Ritchie DJ, et al. Predictors of in-hospital mortality for bloodstream infections caused by Enterobacter species or Citrobacter freundii. Pharmacotherapy. Feb 2007;27(2):191-9. [Medline].

  10. Ye Y, Li JB, Ye DQ, et al. Enterobacter bacteremia: Clinical features, risk factors for multiresistance and mortality in a Chinese University Hospital. Infection. Oct 2006;34(5):252-7. [Medline].

  11. Gallagher PG, Ball WS. Cerebral infarctions due to CNS infection with Enterobacter sakazakii. Pediatr Radiol. 1991;21(2):135-6. [Medline].

  12. Drudy D, Mullane NR, Quinn T, et al. Enterobacter sakazakii: an emerging pathogen in powdered infant formula. Clin Infect Dis. Apr 1 2006;42(7):996-1002. [Medline].

  13. Iversen C, Lehner A, Mullane N, Marugg J, Fanning S, Stephan R, et al. Identification of "Cronobacter" spp. (Enterobacter sakazakii). J Clin Microbiol. Nov 2007;45(11):3814-6. [Medline].

  14. Palmer DL, Kuritsky JN, Lapham SC, et al. Enterobacter mediastinitis following cardiac surgery. Infect Control. Mar 1985;6(3):115-9. [Medline].

  15. Tunkel AR, Fisch MJ, Schlein A, et al. Enterobacter endocarditis. Scand J Infect Dis. 1992;24(2):233-40. [Medline].

  16. Durand ML, Calderwood SB, Weber DJ, et al. Acute bacterial meningitis in adults. A review of 493 episodes. N Engl J Med. Jan 7 1993;328(1):21-8. [Medline].

  17. Maki DG, Weise CE, Sarafin HW. A semiquantitative culture method for identifying intravenous-catheter-related infection. N Engl J Med. Jun 9 1977;296(23):1305-9. [Medline].

  18. Paterson DL. Resistance in gram-negative bacteria: enterobacteriaceae. Am J Med. Jun 2006;119(6 Suppl 1):S20-8; discussion S62-70. [Medline].

  19. Ratnam I, Franklin C, Spelman DW. In vitro activities of 'new' and 'conventional' antibiotics against multi-drug resistant Gram negative bacteria from patients in the intensive care unit. Pathology. Dec 2007;39(6):586-8. [Medline].

  20. Reinert RR, Low DE, Rossi F, et al. Antimicrobial susceptibility among organisms from the Asia/Pacific Rim, Europe and Latin and North America collected as part of TEST and the in vitro activity of tigecycline. J Antimicrob Chemother. Nov 2007;60(5):1018-29. [Medline].

  21. Halstead DC, Abid J, Dowzicky MJ. Antimicrobial susceptibility among Acinetobacter calcoaceticus-baumannii complex and Enterobacteriaceae collected as part of the Tigecycline Evaluation and Surveillance Trial. J Infect. Jul 2007;55(1):49-57. [Medline].

  22. DiPersio JR, Dowzicky MJ. Regional variations in multidrug resistance among Enterobacteriaceae in the USA and comparative activity of tigecycline, a new glycylcycline antimicrobial. Int J Antimicrob Agents. May 2007;29(5):518-27. [Medline].

  23. Ritchie DJ, Alexander BT, Finnegan PM. New antimicrobial agents for use in the intensive care unit. Infect Dis Clin North Am. Sep 2009;23(3):665-81. [Medline].

  24. Jacoby GA. AmpC beta-lactamases. Clin Microbiol Rev. Jan 2009;22(1):161-82, Table of Contents. [Medline].

  25. Bush K, Jacoby GA, Medeiros AA. A functional classification scheme for beta-lactamases and its correlation with molecular structure. Antimicrob Agents Chemother. Jun 1995;39(6):1211-33. [Medline].

  26. Woodford N, Dallow JW, Hill RL, et al. Ertapenem resistance among Klebsiella and Enterobacter submitted in the UK to a reference laboratory. Int J Antimicrob Agents. Apr 2007;29(4):456-9. [Medline].

  27. Souli M, Kontopidou FV, Papadomichelakis E, et al. Clinical experience of serious infections caused by Enterobacteriaceae producing VIM-1 metallo-beta-lactamase in a Greek University Hospital. Clin Infect Dis. Mar 15 2008;46(6):847-54. [Medline].

  28. Pintado V, San Miguel LG, Grill F, et al. Intravenous colistin sulphomethate sodium for therapy of infections due to multidrug-resistant gram-negative bacteria. J Infect. Mar 2008;56(3):185-90. [Medline].

  29. Gupta S, Govil D, Kakar PN, Prakash O, Arora D, Das S. Colistin and polymyxin B: A re-emergence. Indian J Crit Care Med. Apr-Jun 2009;13(2):49-53. [Medline].

  30. Lo-Ten-Foe JR, de Smet AM, Diederen BM, et al. Comparative evaluation of the VITEK 2, disk diffusion, etest, broth microdilution, and agar dilution susceptibility testing methods for colistin in clinical isolates, including heteroresistant Enterobacter cloacae and Acinetobacter baumannii strains. Antimicrob Agents Chemother. Oct 2007;51(10):3726-30. [Medline].

  31. Gales AC, Jones RN, Sader HS. Global assessment of the antimicrobial activity of polymyxin B against 54 731 clinical isolates of Gram-negative bacilli: report from the SENTRY antimicrobial surveillance programme (2001-2004). Clin Microbiol Infect. Apr 2006;12(4):315-21. [Medline].

  32. Walkty A, DeCorby M, Nichol K, Karlowsky JA, Hoban DJ, Zhanel GG. In vitro activity of colistin (polymyxin E) against 3,480 isolates of gram-negative bacilli obtained from patients in Canadian hospitals in the CANWARD study, 2007-2008. Antimicrob Agents Chemother. Nov 2009;53(11):4924-6. [Medline].

  33. Hawser SP, Bouchillon SK, Hoban DJ, Badal RE. In vitro susceptibilities of aerobic and facultative anaerobic Gram-negative bacilli from patients with intra-abdominal infections worldwide from 2005-2007: results from the SMART study. Int J Antimicrob Agents. Dec 2009;34(6):585-8. [Medline].

  34. Bassetti M, Righi E, Fasce R, et al. Efficacy of ertapenem in the treatment of early ventilator-associated pneumonia caused by extended-spectrum beta-lactamase-producing organisms in an intensive care unit. J Antimicrob Chemother. Aug 2007;60(2):433-5. [Medline].

  35. Abbott SL, Janda JM. Enterobacter cancerogenus ("Enterobacter taylorae") infections associated with severe trauma or crush injuries. Am J Clin Pathol. Mar 1997;107(3):359-61. [Medline].

  36. Alhambra A, Cuadros JA, Cacho J, et al. In vitro susceptibility of recent antibiotic-resistant urinary pathogens to ertapenem and 12 other antibiotics. J Antimicrob Chemother. Jun 2004;53(6):1090-4. [Medline].

  37. Caplan ES, Hoyt NJ. Identification and treatment of infections in multiply traumatized patients. Am J Med. Jul 15 1985;79(1A):68-76. [Medline].

  38. Clark NM, Patterson J, Lynch JP 3rd. Antimicrobial resistance among gram-negative organisms in the intensive care unit. Curr Opin Crit Care. Oct 2003;9(5):413-23. [Medline].

  39. Cosgrove SE, Kaye KS, Eliopoulous GM, et al. Health and economic outcomes of the emergence of third-generation cephalosporin resistance in Enterobacter species. Arch Intern Med. Jan 28 2002;162(2):185-90. [Medline].

  40. Cunha BA. Antibiotic Essentials. 9th ed. Sudbury, MA: Jones & Bartlett; 2010.

  41. Cunha BA. Enterobacter: Colonization & infection. Infect Dis Pract. 1999;23:41-3.

  42. Cunha BA. Once-daily tigecycline therapy of multidrug-resistant and non-multidrug-resistant gram-negative bacteremias. J Chemother. Apr 2007;19(2):232-3. [Medline].

  43. Cunha BA. Pharmacokinetic considerations regarding tigecycline for multidrug-resistant (MDR) Klebsiella pneumoniae or MDR Acinetobacter baumannii urosepsis. J Clin Microbiol. May 2009;47(5):1613. [Medline].

  44. Cunha BA, McDermott B, Nausheen S. Single daily high-dose tigecycline therapy of a multidrug-resistant (MDR) Klebsiella pneumoniae and Enterobacter aerogenes nosocomial urinary tract infection. J Chemother. Dec 2007;19(6):753-4. [Medline].

  45. Cunha BA, Theodoris AC, Yannelli B. Enterobacter cloacae graft infection/bacteremia in a hemodialysis patient. Am J Infect Control. Apr 2000;28(2):181-3. [Medline].

  46. De Champs C, Sirot D, Chanal C, et al. A 1998 survey of extended-spectrum beta-lactamases in Enterobacteriaceae in France. The French Study Group. Antimicrob Agents Chemother. Nov 2000;44(11):3177-9. [Medline].

  47. Donati L, Scamazzo F, Gervasoni M, et al. Infection and antibiotic therapy in 4000 burned patients treated in Milan, Italy, between 1976 and 1988. Burns. Aug 1993;19(4):345-8. [Medline].

  48. Foster DR, Rhoney DH. Enterobacter meningitis: organism susceptibilities, antimicrobial therapy and related outcomes. Surg Neurol. Jun 2005;63(6):533-7; discussion 537. [Medline].

  49. Fritsche TR, Stilwell MG, Jones RN. Antimicrobial activity of doripenem (S-4661): a global surveillance report (2003). Clin Microbiol Infect. Dec 2005;11(12):974-84. [Medline].

  50. Fritsche TR, Strabala PA, Sader HS, et al. Activity of tigecycline tested against a global collection of Enterobacteriaceae, including tetracycline-resistant isolates. Diagn Microbiol Infect Dis. Jul 2005;52(3):209-13. [Medline].

  51. Gallagher PG. Enterobacter bacteremia in pediatric patients. Rev Infect Dis. Sep-Oct 1990;12(5):808-12. [Medline].

  52. Hanna H, Afif C, Alakech B, Boktour M, et al. Central venous catheter-related bacteremia due to gram-negative bacilli: significance of catheter removal in preventing relapse. Infect Control Hosp Epidemiol. Aug 2004;25(8):646-9. [Medline].

  53. Hoffmann H, Sturenburg E, Heesemann J, et al. Prevalence of extended-spectrum beta-lactamases in isolates of the Enterobacter cloacae complex from German hospitals. Clin Microbiol Infect. Apr 2006;12(4):322-30. [Medline].

  54. Jiang X, Ni Y, Jiang Y, et al. Outbreak of infection caused by Enterobacter cloacae producing the novel VEB-3 beta-lactamase in China. J Clin Microbiol. Feb 2005;43(2):826-31. [Medline].

  55. Kang CI, Kim SH, Park WB, et al. Bloodstream infections caused by Enterobacter species: predictors of 30-day mortality rate and impact of broad-spectrum cephalosporin resistance on outcome. Clin Infect Dis. Sep 15 2004;39(6):812-8. [Medline].

  56. Kaye KS, Cosgrove S, Harris A, et al. Risk factors for emergence of resistance to broad-spectrum cephalosporins among Enterobacter spp. Antimicrob Agents Chemother. Sep 2001;45(9):2628-30. [Medline].

  57. Larson EL, Cimiotti JP, Haas J, et al. Gram-negative bacilli associated with catheter-associated and non-catheter-associated bloodstream infections and hand carriage by healthcare workers in neonatal intensive care units. Pediatr Crit Care Med. Jul 2005;6(4):457-61. [Medline].

  58. Leverstein-van Hall MA, Blok HE, et al. Extensive hospital-wide spread of a multidrug-resistant enterobacter cloacae clone, with late detection due to a variable antibiogram and frequent patient transfer. J Clin Microbiol. Feb 2006;44(2):518-24. [Medline].

  59. Liu CP, Wang NY, Lee CM, et al. Nosocomial and community-acquired Enterobacter cloacae bloodstream infection: risk factors for and prevalence of SHV-12 in multiresistant isolates in a medical centre. J Hosp Infect. Sep 2004;58(1):63-77. [Medline].

  60. Livermore DM. beta-Lactamases in laboratory and clinical resistance. Clin Microbiol Rev. Oct 1995;8(4):557-84. [Medline].

  61. Livermore DM, Oakton KJ, Carter MW, et al. Activity of ertapenem (MK-0826) versus Enterobacteriaceae with potent beta-lactamases. Antimicrob Agents Chemother. Oct 2001;45(10):2831-7. [Medline].

  62. Luzzaro F, Docquier JD, Colinon C, et al. Emergence in Klebsiella pneumoniae and Enterobacter cloacae clinical isolates of the VIM-4 metallo-beta-lactamase encoded by a conjugative plasmid. Antimicrob Agents Chemother. Feb 2004;48(2):648-50. [Medline].

  63. Markowitz SM, Smith SM, Williams DS. Retrospective analysis of plasmid patterns in a study of burn unit outbreaks of infection due to Enterobacter cloacae. J Infect Dis. Jul 1983;148(1):18-23. [Medline].

  64. Mushtaq S, Ge Y, Livermore DM. Comparative activities of doripenem versus isolates, mutants, and transconjugants of Enterobacteriaceae and Acinetobacter spp. with characterized beta-lactamases. Antimicrob Agents Chemother. Apr 2004;48(4):1313-9. [Medline].

  65. Paterson DL, Rossi F, Baquero F, et al. In vitro susceptibilities of aerobic and facultative Gram-negative bacilli isolated from patients with intra-abdominal infections worldwide: the 2003 Study for Monitoring Antimicrobial Resistance Trends (SMART). J Antimicrob Chemother. Jun 2005;55(6):965-73. [Medline].

  66. Pitout JD, Nordmann P, Laupland KB, et al. Emergence of Enterobacteriaceae producing extended-spectrum beta-lactamases (ESBLs) in the community. J Antimicrob Chemother. Jul 2005;56(1):52-9. [Medline].

  67. Pitout JD, Thomson KS, Hanson ND, et al. Plasmid-mediated resistance to expanded-spectrum cephalosporins among Enterobacter aerogenes strains. Antimicrob Agents Chemother. Mar 1998;42(3):596-600. [Medline].

  68. Ristuccia PA, Cunha BA. Enterobacter. Infect Control. Mar 1985;6(3):124-8. [Medline].

  69. Rupp ME, Fey PD. Extended spectrum beta-lactamase (ESBL)-producing Enterobacteriaceae: considerations for diagnosis, prevention and drug treatment. Drugs. 2003;63(4):353-65. [Medline].

  70. Sader HS, Jones RN, Dowzicky MJ, et al. Antimicrobial activity of tigecycline tested against nosocomial bacterial pathogens from patients hospitalized in the intensive care unit. Diagn Microbiol Infect Dis. Jul 2005;52(3):203-8. [Medline].

  71. Sader HS, Jones RN, Stilwell MG, et al. Tigecycline activity tested against 26,474 bloodstream infection isolates: a collection from 6 continents. Diagn Microbiol Infect Dis. Jul 2005;52(3):181-6. [Medline].

  72. Sanders CC, Sanders WE Jr. beta-Lactam resistance in gram-negative bacteria: global trends and clinical impact. Clin Infect Dis. Nov 1992;15(5):824-39. [Medline].

  73. Sanders WE Jr, Sanders CC. Enterobacter spp.: pathogens poised to flourish at the turn of the century. Clin Microbiol Rev. Apr 1997;10(2):220-41. [Medline].

  74. Siegel JD, Rhinehart E, Jackson M, Chiarello L and the HICPAC. Guideline for Isolation Precautions: Preventing Transmission of Infectious Agents in Healthcare SEttings 2007. Centers for Disease Contol. Available at http://www.cdc.gov/ncidod/dhqp/pdf/guidelines/Isolation2007.pdf. Accessed 1 April 12008.

  75. Siegel JD, Rhinehart E, Jackson M, Chiarello L, HICPAC. Management of Multidrug-Resistant Organisms In Healthcare Settings, 2006. Centers for Disease Control. Available at http://www.cdc.gov/ncidod/dhqp/pdf/ar/mdroGuideline2006.pdf. accessed 1 April 2008.

  76. Tresoldi AT, Padoveze MC, Trabasso P, et al. Enterobacter cloacae sepsis outbreak in a newborn unit caused by contaminated total parenteral nutrition solution. Am J Infect Control. Jun 2000;28(3):258-61. [Medline].

  77. v Dijk Y, Bik EM, Hochstenbach-Vernooij S, v d Vlist GJ, Savelkoul PH, Kaan JA, et al. Management of an outbreak of Enterobacter cloacae in a neonatal unit using simple preventive measures. J Hosp Infect. May 2002;51(1):21-6. [Medline].

  78. Watson JT, Jones RC, Siston AM, et al. Outbreak of catheter-associated Klebsiella oxytoca and Enterobacter cloacae bloodstream infections in an oncology chemotherapy center. Arch Intern Med. Dec 12-26 2005;165(22):2639-43. [Medline].

  79. Wendt C, Lin D, von Baum H. Risk factors for colonization with third-generation cephalosporin-resistant enterobacteriaceae. Infection. Oct 2005;33(5-6):327-32. [Medline].

  80. Wisplinghoff H, Bischoff T, Tallent SM, et al. Nosocomial bloodstream infections in US hospitals: analysis of 24,179 cases from a prospective nationwide surveillance study. Clin Infect Dis. Aug 1 2004;39(3):309-17. [Medline].

 
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Radiograph of an open right tibial fracture in a 21-year-old male marine who was wounded when an improvised explosive device detonated while he was on patrol in Iraq.
 
 
 
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