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Unique Risks and Clinical Outcomes Associated With Extended-Spectrum β-Lactamase Enterobacteriaceae in Veterans With Spinal Cord Injury or Disorder: A Case-Case-Control Study
- Margaret A. Fitzpatrick, Katie J. Suda, Nasia Safdar, Barry Goldstein, Makoto M. Jones, Linda Poggensee, Swetha Ramanathan, Ryan LeWan, Charlesnika T. Evans
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- Journal:
- Infection Control & Hospital Epidemiology / Volume 37 / Issue 7 / July 2016
- Published online by Cambridge University Press:
- 30 March 2016, pp. 768-776
- Print publication:
- July 2016
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- Article
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OBJECTIVES
To describe the burden of extended-spectrum β-lactamase (ESBL) Enterobacteriaceae in veterans with spinal cord injury or disorder (SCI/D), to identify risk factors for ESBL acquisition, and to assess impact on clinical outcomes
DESIGNRetrospective case-case-control study
PATIENTS AND SETTINGVeterans with SCI/D and utilization at a Veterans’ Affairs medical center from January 1, 2012, to December 31, 2013.
METHODSPatients with a positive culture for ESBL Klebsiella pneumoniae, Escherichia coli, or Proteus mirabilis were matched with patients with non-ESBL organisms by organism, facility, and level of care and to uninfected controls by facility and level of care. Inpatients were also matched by time at risk. Univariate and multivariate matched models were assessed for differences in risk factors and outcomes.
RESULTSA total of 492 cases (62.6% outpatients) were matched 1:1 with each comparison group. Recent prior use of fluoroquinolones and prior use of third- and fourth-generation cephalosporins were independently associated with ESBL compared to the non-ESBL group (adjusted odds ratio [aOR], 2.61; 95% confidence interval [CI], 1.77–3.84; P<.001 for fluoroquinolones and aOR, 3.86; 95% CI, 2.06–7.25; P<.001 for third- and fourth-generation cephalosporins) and the control group (aOR, 2.10; 95% CI, 1.29–3.43; P = .003 for fluoroquinolones; and aOR, 3.31; 95% CI, 1.56–7.06; P=.002 for third- and fourth-generation cephalosporins). Although there were no differences in mortality rate, the ESBL group had a longer post-culture length of stay (LOS) than the non-ESBL group (incidence rate ratio, 1.36; 95% CI, 1.13–1.63; P=.001).
CONCLUSIONSAll SCI/D patients with ESBL were more likely to have had recent exposure to fluoroquinolones or third- and fourth-generation cephalosporins, and hospitalized patients were more likely to have increased post-culture LOS. Programs targeted toward reduced antibiotic use in SCI/D patients may prevent subsequent ESBL acquisition.
Infect Control Hosp Epidemiol 2016;37:768–776
Contributors
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- By Ioannis P. Androulakis, Djillali Annane, Gérard Audibert, Lisa L. Barnes, Paolo Bartolomeo, Walter S. Bartynski, David A. Bennett, Nicolas Bruder, Nathan E. Brummel, Steve E. Calvano, Alain Cariou, F. Chretien, Jan Claassen, Colm Cunningham, Souhayl Dahmani, Robert Dantzer, Dimitry S. Davydow, Sanjay V. Desai, E. Wesley Ely, Frédéric Faugeras, Karen J. Ferguson, Brandon Foreman, Sadanand M. Gaikwad, Rebecca F. Gottesman, Maura A. Grega, Richard D. Griffiths, Marion Griton, Stefan D. Gurney, Hebah M. Hefzy, Michael T. Heneka, Dustin M. Hipp, Ramona O. Hopkins, Christopher G. Hughes, James C. Jackson, Christina Jones, Peter W. Kaplan, Keith W. Kelley, Raymond C. Koehler, Matthew A. Koenig, Jan Pieter Konsman, Felix Kork, John P. Kress, Stephen F. Lowry, Alawi Luetz, David Luis, Alasdair M. J. MacLullich, Guy M. McKhann, Jean Mantz, Panteleimon D. Mavroudis, Mervyn Maze, Bruno Mégarbane, Lionel Naccache, Dale M. Needham, Pratik P. Pandharipande, Jean-Francois Payen, V. Hugh Perry, Margaret Pisani, C. Rauturier, Benjamin Rohaut, Jennifer Ryan, Robert D. Sanders, Jeremy D. Scheff, Frederic Sedel, Ola A. Selnes, Tarek Sharshar, Martin Siegemund, Yoanna Skrobik, Jamie W. Sleigh, Romain Sonneville, Claudia D. Spies, Luzius A. Steiner, Robert D. Stevens, Raoul Sutter, Fabio Silvio Taccone, Richard E. Temes, Willem A. van Gool, Christel C. Vanbesien, F. Verdonk, Odile Viltart, Julia Wendon, Catherine N. Widmann, Robert S. Wilson
- Edited by Robert D. Stevens, Tarek Sharshar, E. Wesley Ely, Vanderbilt University, Tennessee
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- Book:
- Brain Disorders in Critical Illness
- Published online:
- 05 October 2013
- Print publication:
- 19 September 2013, pp viii-xii
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Chap. 31 - ENDOCRINOLOGIC EMERGENCIES IN DERMATOLOGY
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- By Margaret T. Ryan, Riddle Memorial Hospital, Vincent Savarese, Jefferson Medical College of Thomas Jefferson University, Serge A. Jabbour, Jefferson Medical College of Thomas Jefferson University
- Edited by Ronni Wolf, Batya B. Davidovici, Jennifer L. Parish, Lawrence Charles Parish
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- Book:
- Emergency Dermatology
- Published online:
- 07 September 2011
- Print publication:
- 17 January 2011, pp 298-312
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Summary
ENDOCRINE AND METABOLIC DISEASES, besides affecting other organs, can result in changes in cutaneous function and morphology and can lead to a complex symptomatology. Dermatologists may see some of these skin lesions first, either before the endocrinologist, or even after the internist or specialist has missed the right diagnosis. Because some skin lesions might reflect a life-threatening endocrine or metabolic disorder, identifying the underlying disorder is important, so that patients can receive corrective rather than symptomatic treatment.
In this section, we review a few endocrine and metabolic disorders in which patients may present to the dermatologist with various skin lesions and in which the diagnosis of the underlying condition must be made in a timely fashion before the patient ends up with complications that could be fatal.
HYPERPIGMENTATION AND ADDISON DISEASE
Addison disease, or primary adrenal insufficiency, can be caused by either infiltrative disorders that invade the adrenal cortex or by destructive disorders that attack the adrenal cells. In either etiology, the adrenal cortex is unable to produce and secrete adequate amounts of glucocorticoid and mineralocorticoid hormones. The most common etiology of Addison disease used to be tuberculous granulomatous disease, but with declining infection rates in the developed world, the most common cause of Addison disease today is autoimmune destruction of the adrenal glands. Other less common causes of Addison include other granulomatous fungal infections (histoplasmosis, coccidiomycosis), metastatic carcinoma infiltration of the adrenals, or bilateral adrenal hemorrhage.