Hostname: page-component-78c5997874-lj6df Total loading time: 0 Render date: 2024-11-05T09:54:57.008Z Has data issue: false hasContentIssue false
  • English
  • Français

Moxifloxacin Therapy as a Risk Factor for Clostridium difficile–Associated Disease During an Outbreak: Attempts to Control a New Epidemic Strain

Published online by Cambridge University Press:  02 January 2015

Priscilla Biller ,
Beth Shank ,
Leah Lind ,
Meghan Brennan ,
Lisa Tkatch ,
George Killgore ,
Angela Thompson  and
L. Clifford McDonald
Priscilla Biller
Affiliation:
Holy Spirit Hospital, Camp Hill, Pennsylvania
Beth Shank
Affiliation:
Holy Spirit Hospital, Camp Hill, Pennsylvania
Leah Lind
Affiliation:
Pennsylvania Department of Health, Harrisburg, Pennsylvania
Meghan Brennan
Affiliation:
Centers for Disease Control and Prevention, Atlanta, Georgia
Lisa Tkatch
Affiliation:
Holy Spirit Hospital, Camp Hill, Pennsylvania
George Killgore
Affiliation:
Centers for Disease Control and Prevention, Atlanta, Georgia
Angela Thompson
Affiliation:
Centers for Disease Control and Prevention, Atlanta, Georgia
L. Clifford McDonald*
Affiliation:
Centers for Disease Control and Prevention, Atlanta, Georgia
*
Centers for Disease Control and Prevention, 1600 Clifton Road, MS A35, Atlanta, GA 30333 ([email protected])
Get access Rights & Permissions [Opens in a new window]

Abstract

An outbreak of Clostridium difficile-associated disease (CDAD) caused by the epidemic North American pulsed-field gel electrophoresis type 1 (NAP1) strain began after a formulary change from levofloxacin to moxifloxacin. Cases of CDAD were associated with moxifloxacin use, but a formulary change back to levofloxacin failed to reduce rates of disease. Substituting use of one fluoroquinolone with use of another without also controlling the overall use of drugs from this class is unlikely to control outbreaks caused by the NAP1 strain of C. difficile.

Type
Concise Communication
Information
Infection Control & Hospital Epidemiology , Volume 28 , Issue 2 , February 2007 , pp. 198 - 201
Copyright
Copyright © The Society for Healthcare Epidemiology of America 2007

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

1.McDonald, LC, Owings, M, Jernigan, DB. Increasing incidence of Clostridium difficile-associated disease in US short-stay hospitals, 1996-2003. Emerg Infect Dis 2006;12:409–415.Google Scholar
2.Layton, BA, McDonald, LC, Gerding, DN, Liedtke, LA, Strausbaugh, LJ. Perceived increases in the incidence and severity of Clostridium difficile disease: an emerging threat that continues to unfold. In: Proceedings of the 15th Annual Scientific Meeting of the Society for Healthcare Epidemiology of America, Los Angeles, CA, April 4-9, 2005. Abstract.Google Scholar
3.Eggertson, L, Sibbald, B. Hospitals battling outbreaks of Clostridium difficile. CMAJ 2004;171:19–21.Google Scholar
4.McDonald, LC, Killgore, GE, Thompson, A, et al. An epidemic, toxin gene-variant strain of Clostridium difficile. N Engl J Med 2005;353:2433–2441.CrossRefGoogle ScholarPubMed
5.Warny, M, Pepin, J, Fang, A, et al. Toxin production by an emerging strain of Clostridium difficile associated with outbreaks of severe disease in North America and Europe. Lancet 2005;366:1079–1084.Google Scholar
6.Gaynes, R, Rimland, D, Killum, E, et al. Outbreak of Clostridium difficile infection in a long-term care facility: association with gatifloxacin use. Clin Infect Dis 2004;38:640–645.Google Scholar
7.Muto, CA, Pokrywka, MF, Shutt, K, et al. A large outbreak of Clostridium difficile-associated disease with an unexpected proportion of deaths and colectomies at a teaching hospital following increased fluoroquinolone use. Infect Control Hosp Epidemiol 2005;26:273–280.CrossRefGoogle Scholar
8.Allen, SD, Emery, CL, Lyerly, DM. Clostridium. In: Murray, PR, Baron, EJ, Jorgensen, JH, Pfaller, MA, Yolken, RH, eds. Manual of Clinical Microbiology. 8th ed. Washington, DC: American Society for Microbiology; 2003:845–847.Google Scholar
9.Rupnik, M, Avesani, V, Jane, M, Eichel-Streiber, C, Delmee, M. A novel toxinotyping scheme and correlation of toxinotypes with serogroups of Clostridium difficile isolates. J Clin Microbiol 1998;36:2240–2247.CrossRefGoogle ScholarPubMed
10.Fawley, WN, Wilcox, MH. Pulsed-field gel electrophoresis can yield DNA fingerprints of degradation-susceptible Clostridium difficile strains. J Clin Microbiol 2002;40:3546–3547.Google Scholar
11.Stubbs, S, Rupnik, M, Gibert, M, Brazier, J, Duerden, B, Popoff, M. Production of actin-specific ADP-ribosyltransferase (binary toxin) by strains of Clostridium difficile. FEMS Microbiol Lett 2000;186:307–312.CrossRefGoogle ScholarPubMed
12.Spigaglia, P, Mastrantonio, P. Molecular analysis of the pathogenicity locus and polymorphism in the putative negative regulator of toxin production (TcdC) among Clostridium difficile clinical isolates. J Clin Microbiol 2002;40:3470–3475.Google Scholar
13.National Committee for Clinical Laboratory Standards. Methods for Antimicrobial Susceptibility Testing of Anaerobic Bacteria. 6th ed. Wayne, PA: National Committee for Clinical Laboratory Standards; 2004. Approved standard M11-A6.Google Scholar
14.Elixhauser, A, Steiner, C, Harris, DR, Coffey, RM. Comorbidity measures for use with administrative data. Med Care 1998;36:8–27.Google Scholar
15.Gerding, DN, Johnson, S, Peterson, LR, Mulligan, ME, Silva, J Jr. Clostridium difficile-associated diarrhea and colitis. Infect Control Hosp Epidemiol 1995;16:459–477.Google Scholar
16.Centers for Disease Control and Prevention. Clostridium difficile—information for healthcare providers. Atlanta, GA: Centers for Disease Control and Prevention; 2005. Available at: http://www.cdc.gov/ncidod/ dhqp/id_CdiffFAQ_HCP.html. Accessed March 2006.Google Scholar