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Persistence of Skin Contamination and Environmental Shedding of Clostridium difficile during and after Treatment of C. difficile Infection

Part of: BARRY FARR AWARD RECIPIENTS

Published online by Cambridge University Press:  02 January 2015

Ajay K. Sethi ,
Wafa N. Al-Nassir ,
Michelle M. Nerandzic ,
Greg S. Bobulsky  and
Curtis J. Donskey
Ajay K. Sethi
Affiliation:
Departments of Epidemiology and Biostatistics, Cleveland Veterans Affairs Medical Center, Cleveland, Ohio
Wafa N. Al-Nassir
Affiliation:
Infectious Diseases, Cleveland Veterans Affairs Medical Center, Cleveland, Ohio
Michelle M. Nerandzic
Affiliation:
University Hospitals of Cleveland, Case Western, Reserve University School of Medicine, and the Research Service, Cleveland Veterans Affairs Medical Center, Cleveland, Ohio
Greg S. Bobulsky
Affiliation:
University Hospitals of Cleveland, Case Western, Reserve University School of Medicine, and the Research Service, Cleveland Veterans Affairs Medical Center, Cleveland, Ohio
Curtis J. Donskey*
Affiliation:
University Hospitals of Cleveland, Case Western, Reserve University School of Medicine, and the Research Service, Cleveland Veterans Affairs Medical Center, Cleveland, Ohio Geriatric Research, Education, and Clinical Center, Cleveland Veterans Affairs Medical Center, Cleveland, Ohio
*
Infectious Diseases Section (1110 W), Cleveland VA Medical Center, 10701 East Boulevard, Cleveland, Ohio 44106 ([email protected])
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Extract

Background.

Current guidelines for control of Clostridium difficile infection (CDI) suggest that contact precautions be discontinued after diarrhea resolves. However, limited information is available regarding the frequency of skin contamination and environmental shedding of C. difficile during and after treatment.

Design.

We conducted a 9-month prospective, observational study involving 52 patients receiving therapy for CDI. Stool samples, skin (chest and abdomen) samples, and samples from environmental sites were cultured for C. difficile before, during, and after treatment. Polymerase chain reaction ribotyping was performed to determine the relatedness of stool, skin, and environmental isolates.

Results.

Fifty-two patients with CDI were studied. C. difficile was suppressed to undetectable levels in stool samples from most patients during treatment; however, 1-4 weeks after treatment, 56% of patients who had samples tested were asymptomatic carriers of C. difficile. The frequencies of skin contamination and environmental shedding remained high at the time of resolution of diarrhea (60% and 37%, respectively), were lower at the end of treatment (32% and 14%, respectively), and again increased 1-4 weeks after treatment (58% and 50%, respectively). Skin and environmental contamination after treatment was associated with use of antibiotics for non-CDI indications. Ninety-four percent of skin isolates and 82% of environmental isolates were genetically identical to concurrent stool isolates.

Conclusions.

Skin contamination and environmental shedding of C. difficile often persist at the time of resolution of diarrhea, and recurrent shedding is common 1-4 weeks after therapy. These results provide support for the recommendation that contact precautions be continued until hospital discharge if rates of CDI remain high despite implementation of standard infection-control measures.

Type
Original Articles
Information
Infection Control & Hospital Epidemiology , Volume 31 , Issue 1 , January 2010 , pp. 21 - 27
Copyright
Copyright © The Society for Healthcare Epidemiology of America 2010

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References

1.Poutanen, SM, Simor, AE. Clostridium difficile-associated diarrhea in adults. CMAJ 2004;171:51–58.CrossRefGoogle ScholarPubMed
2.McDonald, LC, Killgore, GE, Thompson, A, et al. An epidemic, toxin gene-variant strain of Clostridium diffkile. N Engl J Med 2005;353:2433–2441.CrossRefGoogle Scholar
3.Loo, VG, Poirier, L, Miller, MA, et al. A predominandy clonal multi-institutional outbreak of Clostridium difficile-associated diarrhea with high morbidity and mortality. N Engl J Med 2005;353:2442–2449.CrossRefGoogle ScholarPubMed
4.Muto, CA, Pokrywka, M, Shutt, K, et al. A large outbreak of Clostridium difficile-associated disease with at unexpected proportion of deaths and colectomies at a teaching hospital following increased fluoroquinolone use. Infect Control Hosp Epidemiol 2005;26:273–280.Google Scholar
5.Gerding, DN, Johnson, S, Peterson, LR, Mulligan, ME, Silva, J. Clostridium difficile-associated diarrhea and colitis. Infect Control Hosp Epidemiol 1995;16:459–477.Google Scholar
6.Dubberke, ER, Gerding, DN, Classen, D, et al. Strategies to prevent Clostridium difficile infections in acute care hospitals. Infect Control Hosp Epidemiol 2008;29:S81-S92.Google Scholar
7.McFarland, LV, Elmer, GW, Surawicz, CM. Breaking the cycle: treatment strategies for 163 cases of recurrent Clostridium difficile disease. Am J Gastroenterol 2002;97:1769–1775.CrossRefGoogle ScholarPubMed
8.Bobulsky, G, Al-Nassir, WN, Riggs, MM, Sethi, AK, Donskey, CJ. Clostridium difficile skin contamination in patients with C. diffidle-associated disease. Clin Infect Dis 2008;46:447–450.CrossRefGoogle Scholar
9.Al-Nassir, WN, Sethi, AK, Nerandzic, MM, Bobulsky, G, Jump, RL, Donskey, CJ. Comparison of clinical and microbiological response to treatment of Clostridium difficile-associated disease with metronidazole and vancomycin. Clin Infect Dis 2008;47:56–62.Google Scholar
10.Bidet, P, Lalande, V, Salauze, B, et al. Comparison of PCR-ribotyping, arbitrarily primed PCR, and pulsed-field gel electrophoresis for typing Clostridium difficile. J Clin Microbiol 2000;38:2484–2487.Google Scholar
11.Terhes, G, Urban, E, Sold, J, Hamid, KA, Nagy, E. Community-acquired Clostridium difficile diarrhea caused b. binary toxin, toxin A, and toxin? gene-positive isolates in Hungary. J Clin Microbiol 2004;42:4316–4318.Google Scholar
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 isolates. J Clin Microbiol 2002;40:3470–3475.CrossRefGoogle Scholar
13.Samore, MH, Vekataraman, L, DeGirolami, PC, Arbeit, RD, Karchmer, AW. Clinical and molecular epidemiology of sporadic and clustered cases of nosocomial Clostridium difficile. Am J Med 1996;100:32–40.CrossRefGoogle ScholarPubMed
14.Riggs, MM, Sethi, AK, Zabarsky, TF, Eckstein, EC, Jump, RL, Donskey, CJ. Asymptomatic carriers are a potential source for transmission of epidemic and nonepidemic Clostridium difficile strains among long-term care facility residents. Clin Infect Dis 2007;45:992–998.CrossRefGoogle ScholarPubMed
15.Muto, CA, Blank, MK, Marsh, JW, et al. Control of at outbreak of infections with the hypervirulent Clostridium difficile BI strain in a University Hospital using a comprehensive bundle approach. Clin Infect Dis 2007;45:1266–1273.CrossRefGoogle Scholar
16.Valiquette, L, Cossette, B, Garant, MP, Diab, H, Pepin, J. Impact of a reduction in high-risk antibiotics of the course of an epidemic of Clostridium difficile-associated disease caused b. the hypervirulent NAPI/027 strain. Clin Infect Dis 2007;45:S112–S121.Google Scholar
17.Vernon, MO, Hayden, MK, Trick, WE, Hayes, RA, Blom, DW, Weinstein, RA. Chlorhexidine gluconate to cleanse patients in a medical intensive care unit: The effectiveness of source control to reduce the bioburden of vancomycin-resistant enterococci. Arch Intern Med 2006;166:306–312.CrossRefGoogle Scholar
18.Duckro, AN, Blom, DW, Lyle, EA, Weinstein, RA, Hayden, MK. Transfer of vancomycin-resistant enterococci via health care worker hands. Arch Intern Med 2005;165:302–307.Google Scholar