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Molecular Epidemiology of Clostridium difficile Infections in Children: A Retrospective Cohort Study

Published online by Cambridge University Press:  23 January 2015

Larry K. Kociolek ,
Sameer J. Patel ,
Stanford T. Shulman  and
Dale N. Gerding
Larry K. Kociolek*
Affiliation:
Department of Pediatrics, Division of Infectious Diseases, Ann & Robert H. Lurie Children’s Hospital of Chicago and Northwestern University Feinberg School of Medicine, Chicago, Illinois
Sameer J. Patel
Affiliation:
Department of Pediatrics, Division of Infectious Diseases, Ann & Robert H. Lurie Children’s Hospital of Chicago and Northwestern University Feinberg School of Medicine, Chicago, Illinois
Stanford T. Shulman
Affiliation:
Department of Pediatrics, Division of Infectious Diseases, Ann & Robert H. Lurie Children’s Hospital of Chicago and Northwestern University Feinberg School of Medicine, Chicago, Illinois
Dale N. Gerding
Affiliation:
Department of Medicine, Hines VA Hospital, Hines, Illinois Loyola University of Chicago, Stritch School of Medicine, Maywood, Illinois
*
Address correspondence to Larry K. Kociolek, MD, 225 E. Chicago Ave, Box 20, Chicago, IL 60611 (Larry-Kociolek@northwestern.edu).
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Abstract

OBJECTIVE

The molecular epidemiology of pediatric Clostridium difficile infection (CDI) is poorly understood. We aimed to identify the restriction endonuclease analysis (REA) groups causing CDI and to determine risk factors and outcomes associated with CDI caused by epidemic strains in children.

DESIGN

Retrospective cohort study

PATIENTS

Inpatients and outpatients >1 year old receiving care between December 2012 and December 2013

SETTING

An academic children’s hospital in Chicago, Illinois

METHODS

C. difficile PCR-positive stools were cultured, and C. difficile isolates were typed by REA. REA of isolates from patients with multiple CDIs was performed to differentiate relapse (infection with same strain) from reinfection (different strains) irrespective of time between CDIs.

RESULTS

A total of 189 CDIs occurred among 145 patients. REA groups were widely distributed. The BI/NAP1/027 strain caused CDI in only 1 patient. DH/NAP11/106, the predominant epidemic strain identified, was associated with the use of third- or fourth-generation cephalosporins (risk ratio [RR], 3.2; 95% confidence interval [CI], 1.1–9.9; P=.04). CDI relapse commonly occurred up to 20 weeks later. Compared with CDI caused by non-DH/NAP11/106 strains, CDI caused by DH/NAP11/106 was more likely to result in multiple CDI relapses (40% vs 8%; P=.05) among children with multiple CDIs.

CONCLUSIONS

REA identified the exceedingly low prevalence of BI/NAP1/027 and the high prevalence of DH/NAP11/106, a common epidemic strain in the United Kingdom that is less often reported in the United States. CDI relapse commonly occurred up to 20 weeks from the previous CDI. Defining recurrent CDI as that occurring only within 8 weeks of the original infection may lead to misclassification of some recurrent CDIs as new CDIs in children.

Infect Control Hosp Epidemiol 2015;00(0): 1–7

Type
Original Articles
Information
Infection Control & Hospital Epidemiology , Volume 36 , Issue 4 , April 2015 , pp. 445 - 451
Copyright
© 2015 by The Society for Healthcare Epidemiology of America. All rights reserved 

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Footnotes

PREVIOUS PRESENTATION. The findings reported in the present study were presented as abstracts at ID Week 2014 (October 10, 2014, in Philadelphia, Pennsylvania).

References

1. Kelly, CP, Lamont, JT. Clostridium difficile—more difficult than ever. N Engl J Med 2008;359:1932–1940.CrossRefGoogle ScholarPubMed
2. 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
3. Benson, L, Song, X, Campos, J, Singh, N. Changing epidemiology of Clostridium difficile-associated disease in children. Infect Control Hosp Epidemiol 2007;28:1233–1235.Google Scholar
4. Kim, J, Smathers, SA, Prasad, P, Leckerman, KH, Coffin, S, Zaoutis, T. Epidemiological features of Clostridium difficile-associated disease among inpatients at children's hospitals in the United States, 2001–2006. Pediatrics 2008;122:1266–1270.CrossRefGoogle ScholarPubMed
5. Zilberberg, MD, Tillotson, GS, McDonald, C. Clostridium difficile infections among hospitalized children, United States, 1997–2006. Emerg Infect Dis 2010;16:604–609.Google Scholar
6. Nylund, CM, Goudie, A, Garza, JM, Fairbrother, G, Cohen, MB. Clostridium difficile infection in hospitalized children in the United States. Arch Pediatr Adolesc Med 2011;165:451–457.CrossRefGoogle ScholarPubMed
7. Freeman, J, Bauer, MP, Baines, SD, et al. The changing epidemiology of Clostridium difficile infections. Clin Microbiol Rev 2010;23:529–549.Google Scholar
8. Tamma, PD, Sandora, TJ. Clostridium difficile infection in children: current state and unanswered questions. J Pediatric Infect Dis Soc 2012;1:230–243.Google Scholar
9. Kim, J, Shaklee, JF, Smathers, S, et al. Risk factors and outcomes associated with severe Clostridium difficile infection in children. Pediatr Infect Dis J 2012;31:134–138.CrossRefGoogle ScholarPubMed
10. Khanna, S, Baddour, LM, Huskins, WC, et al. The epidemiology of Clostridium difficile infection in children: a population-based study. Clin Infect Dis 2013;56:1401–1406.Google Scholar
11. Tschudin-Sutter, S, Tamma, PD, Milstone, AM, Perl, TM. Predictors of first recurrence of Clostridium difficile infections in children. Pediatr Infect Dis J 2014;33:414–416.Google Scholar
12. Toltzis, P, Kim, J, Dul, M, Zoltanski, J, Smathers, S, Zaoutis, T. Presence of the epidemic North American pulsed field type 1 Clostridium difficile strain in hospitalized children. J Pediatr 2009;154:607–608.Google Scholar
13. Wendt, JM, Cohen, JA, Mu, Y, et al. Clostridium difficile infection among children across diverse US geographic locations. Pediatrics 2014;133:651–658.Google Scholar
14. Shin, S, Kim, M, Kim, M, et al. Evaluation of the Xpert Clostridium difficile assay for the diagnosis of Clostridium difficile infection. Ann Lab Med 2012;32:355–358.Google Scholar
15. Wilson, KH, Kennedy, MJ, Fekety, FR. Use of sodium taurocholate to enhance spore recovery on a medium selective for Clostridium difficile . J Clin Microbiol 1982;15:443–446.Google Scholar
16. Clabots, CR, Gerding, SJ, Olson, MM, Peterson, LR, Gerding, DN. Detection of asymptomatic Clostridium difficile carriage by an alcohol shock procedure. J Clin Microbiol 1989;27:2386–2387.Google Scholar
17. Clabots, CR, Johnson, S, Bettin, KM, et al. Development of a rapid and efficient restriction endonuclease analysis typing system for Clostridium difficile and correlation with other typing systems. J Clin Microbiol 1993;31:1870–1875.Google Scholar
18. McDonald, LC, Coignard, B, Dubberke, E, et al. Recommendations for surveillance of Clostridium difficile-associated disease. Infect Control Hosp Epidemiol 2007;28:140–145.CrossRefGoogle ScholarPubMed
19. Kamboj, M, Khosa, P, Kaltsas, A, Babady, NE, Son, C, Sepkowitz, KA. Relapse versus reinfection: surveillance of Clostridium difficile infection. Clin Infect Dis 2011;53:1003–1006.CrossRefGoogle ScholarPubMed
20. Black, SR, Weaver, KN, Jones, RC, et al. Clostridium difficile outbreak strain BI is highly endemic in Chicago area hospitals. Infect Control Hosp Epidemiol 2011;32:897–902.Google Scholar
21. Belmares, J, Johnson, S, Parada, JP, et al. Molecular epidemiology of Clostridium difficile over the course of 10 years in a tertiary care hospital. Clin Infect Dis 2009;49:1141–1147.Google Scholar
22. Johnson, S. Editorial commentary: changing epidemiology of Clostridium difficile and emergence of new virulent strains. Clin Infect Dis 2014;58:1731–1733.Google Scholar
23. Sundram, F, Guyot, A, Carboo, I, Green, S, Lilaonitkul, M, Scourfield, A. Clostridium difficile ribotypes 027 and 106: clinical outcomes and risk factors. J Hosp Infect 2009;72:111–118.CrossRefGoogle ScholarPubMed
24. Dionne, LL, Raymond, F, Corbeil, J, Longtin, J, Gervais, P, Longtin, Y. Correlation between Clostridium difficile bacterial load, commercial real-time PCR cycle thresholds, and results of diagnostic tests based on enzyme immunoassay and cell culture cytotoxicity assay. J Clin Microbiol 2013;51:3624–3630.Google Scholar
25. Hensgens, MP, Goorhuis, A, Dekkers, OM, Kuijper, EJ. Time interval of increased risk for Clostridium difficile infection after exposure to antibiotics. J Antimicrob Chemother 2012;67:742–748.Google Scholar
26. Killgore, G, Thompson, A, Johnson, S, et al. Comparison of seven techniques for typing international epidemic strains of Clostridium difficile: restriction endonuclease analysis, pulsed-field gel electrophoresis, PCR-ribotyping, multilocus sequence typing, multilocus variable-number tandem-repeat analysis, amplified fragment length polymorphism, and surface layer protein A gene sequence typing. J Clin Microbiol 2008;46:431–437.Google Scholar
27. Marsh, JW, Arora, R, Schlackman, JL, Shutt, KA, Curry, SR, Harrison, LH. Association of relapse of Clostridium difficile disease with BI/NAP1/027. J Clin Microbiol 2012;50:4078–4082.Google Scholar
28. Tschudin-Sutter, S, Tamma, PD, Milstone, AM, Perl, TM. The prediction of complicated Clostridium difficile infections in children. Infect Control Hosp Epidemiol 2014;35:901–903.Google Scholar
29. Kociolek, LK, Patel, SJ, Shulman, ST, Gerding, DN. Concomitant medical conditions and therapies preclude accurate classification of children with severe or severe complicated Clostridium difficile infection. J Pediatric Infect Dis Soc 2014; Epub ahead of print.Google Scholar