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Clostridium difficile

Also known as: C.diff, C. difficile; Causes C. difficile infection (CDI) 

Industry of Interest: Healthcare

Classification: Bacteria

Microbiology: Microbiology: Clostridium difficile is a Gram-positive spore forming rod. C. difficile was first identified in the 1930s, but its medical importance as a cause of antibiotic-associated diarrhoea and colitis (inflammation of the colon) was not recognised until the mid-1970s.
C. difficile is now a common cause of antibiotic-associated diarrhoea.  An epidemic clone, called NAP1/027, emerged in the early 2000s and is associated with a dramatic increase in the incidence and severity of C. difficile disease.

Biology

Habitat and transmission: C. difficile is an anaerobic bacterium that produces spores in response to stress. C. difficile resides in anaerobic sections of the human intestines. For reasons that are not well understood, around two thirds of young children carry C. difficile in their gut without developing C. Difficileinfection (CDI). Asymptomatic carriage of C. difficile is much less common in adults – typically only 3-5% of healthy adults and 20-40% of hospitalised adults. C. difficile spores are transmitted by the faecal-oral route. They are difficult to eradicate from the environment and can be spread via the hands of healthcare workers.

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Detection of the C. difficile toxin using enzyme immunoassays (EIA) has been the mainstay of CDI diagnosis. However, recent data indicate that the sensitivity of EIA tests for the C. difficile toxin is poor and can be as low as 50%; PCR-based methods improve the sensitivity of detection and are beginning to replace EIAs. This has resulted in elevated rates of CDI in hospitals where testing has switched to more sensitive methods through improved detection of C. Difficilerather than increased transmission.

Treatment:

Patients with CDI are usually treated with antibiotics (principally vancomycin and metronidazole), which kill the C. difficile cells producing the toxin.6 In severe cases, surgery may be required to remove the colon (colectomy).  Clinical presentations with the NAP1/027 strain appear to be more serious than other C. difficile strains, resulting in increased morbidity and mortality. These clinical properties are associated with increased toxin production and increased resistance to the fluoroquinolones and poor clinical response to metronidazole, the two mainstays of treatment for CDI.   Alternative therapies such as new antibiotics, monoclonal antibodies, a vaccine and novel biotherapeutics (faecal transplant) are being explored.

Prevention and control:

C. difficile spores are particularly hardy and able to survive in the environment for extended periods of time, resist the effects of alcohol gels and some disinfectants, and spread on healthcare workers’ hands. Prevention and control measures include hand hygiene using soap and water, isolation of infected patients, contact precautions (such as glove and gown use), enhanced environmental decontamination and restriction of the use of high-risk antimicrobial agents.  Widespread environmental contamination with C. Difficileoccurs and is difficult to eradicate using conventional methods. Indeed, admission to a room previously occupied by a patient with CDI significantly increases the chances of acquisition.  Several studies indicate that the elimination of C. difficile using Bioquell hydrogen peroxide vapour (HPV) reduces the incidence of CDI.

References:
1. Bartlett, J.G., Moon, N., Chang, T.W., Taylor, N. and Onderdonk, A.B. (1978) Role of Clostridium difficile in antibiotic-associated pseudomembranous colitis. Gastroenterology 75, 778-782.
2. Kuijper, E.J., Coignard, B. and Tull, P. (2006) Emergence of Clostridium difficile-associated disease in North America and Europe. Clin Microbiol Infect 12 Suppl 6, 2-18.
3. Merida, V., Moerman, J., Colaert, J., Lemmens, P. and Vandepitte, J. (1986) Significance of Clostridium difficile and its cytotoxin in children. EurJ Pediatr 144, 494-496.
4. Bartlett, J.G. and Perl, T.M. (2005) The new Clostridium difficile--what does it mean? N Engl J Med 353, 2503-2505.
5. Goldenberg, S.D. and French, G.L. (2011) Diagnostic testing for Clostridium difficile: a  omprehensive survey of laboratories in England. J Hosp Infect 79, 4-7.
6. Aslam, S., Hamill, R.J. and Musher, D.M. (2005) Treatment of Costridium difficile-associated disease: old therapies and new trategies. Lancet Infect Dis 5, 549-557.
7. McDonald, L.C., Killgore, G.E., Thompson, A., Owens, R.C., Jr., Kazakova, S.V., Sambol, S.P., Johnson, S. and Gerding, D.N. (2005) An epidemic, toxin gene-variant strain of Clostridium difficile. N Engl J Med 353, 2433-2441.
8. Pepin, J., Saheb, N., Coulombe, M.A., Alary, M.E., Corriveau, M.P., Authier, S., Leblanc, M., Rivard, G., Bettez, M., Primeau, V., Nguyen, M., Jacob, C.E. and Lanthier, L. (2005) Emergence of fluoroquinolones as the predominant risk factor for Clostridium difficile-associated
diarrhea: a cohort study during an epidemic in Quebec.  Clin Infect Dis 41, 1254-1260.
9. Warny, M., Pepin, J., Fang, A., Killgore, G., Thompson, A., Brazier, J., Frost, E. and McDonald, L.C. (2005) Toxin production by an emerging strain of Clostridium difficile associated with outbreaks of
severe disease in North America and Europe. Lancet 366, 1079-1084.
10. Department of Health and Health Protection Agency (2009) Clostridium difficile: how to deal with the problem.
11. Cohen, S.H., Gerding, D.N., Johnson, S., Kelly, C.P., Loo, V.G., McDonald, L.C., Pepin, J. and Wilcox, M.H. (2010) Clinical practice guidelines for Clostridium difficile infection in adults: 2010 update by the society for healthcare epidemiology of America (SHEA) and the infectious diseases society of America (IDSA). Infect Control Hosp Epidemiol 31, 431-455.
12. Wilcox, M.H., Fawley, W.N., Wigglesworth, N., Parnell, P., Verity, P. and Freeman, J. (2003) Comparison of the effect of detergent versus hypochlorite cleaning on environmental contamination and incidence of Clostridium difficile infection. J Hosp Infect 54, 109-114.
13. Boyce, J.M., Havill, N.L., Otter, J.A., McDonald, L.C., Adams, N.M., Cooper, T., Thompson, A., Wiggs, L., Killgore, G., Tauman, A. and Noble-Wang, J. (2008) Impact of hydrogen peroxide vapor
room decontamination on Clostridium difficile environmental contamination and transmission in a healthcare setting. Infect Control Hosp Epidemiol 29, 723-729.
14. Shaughnessy, M.K., Micielli, R.L., DePestel, D.D., Arndt, J., Strachan, C.L., Welch, K.B. and Chenoweth, C.E. (2011) Evaluation of hospital room assignment and acquisition of Clostridium difficile
infection. Infect Control Hosp Epidemiol 32, 201-206.
15. Manian, F.A., Griesenauer, S. and Senkel, D. (2010) Impact of an intensive terminal cleaning and disinfection (C/D) protocol involving selected hospital rooms on endemic nosocomial infection (NI) rates of common pathogens at a tertiary care medical center. 5th Decennial Meeting of the Society for Healthcare Epidemiology of America (SHEA), Atlanta, GA, USA. Abstract LB6.
16. Cooper, T., O’Leary, M., Yezli, S. and Otter, J.A. (2011) Impact of environmental decontamination using hydrogen peroxide vapour on the incidence of Clostridium difficile infection in one hospital Trust. J Hosp Infect 78, 238-240.
17. Rupnik, M., Wilcox, M.H. and Gerding, D.N. (2009) Clostridium difficile infection: new developments in epidemiology and pathogenesis. Nat Rev Microbiol 7, 526-536.
18. Freeman, J., Bauer, M.P., Baines, S.D., Corver, J., Fawley, W.N., Goorhuis, B., Kuijper, E.J. and Wilcox, M.H. (2010) The changing epidemiology of Clostridium difficile infections. Clin Microbiol Rev 23, 529-549.

 

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