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== Historical Perspective ==
==Overview==
On June 4, 2004, two outbreaks of a highly virulent strain of this bacterium were reported in Montreal, Quebec and Calgary, Alberta, in Canada. Sources put the death count as low as 36 and as high as 89, with approximately 1,400 cases in 2003 and within the first few months of 2004. ''C. difficile'' infections continued to be a problem in the Quebec health care system in late 2004. As of March 2005, it had spread into the Toronto, Ontario area, hospitalizing 10 people. One died while the others were being discharged.
''Clostridium difficile'' was first isolated in 1935 during an experiment from [[fecal extract]]s of healthy [[neonate]]s. The association between ''C. difficile'' and antibiotic-associated pseudomembranous colitis was first made in 1978. In 2003, a resistant, [[hypervirulent strain]] of ''C. difficile'' (NAP/BI/027 strain) with increased synthesis of toxins A and B was first identified.


A similar outbreak took place at Stoke Mandeville Hospital in the United Kingdom between 2003 and 2005. The local [[epidemiology]] of ''C. difficile'' may offer clues on how its spread may relate to the amount of time a patient spends in hospital and/or a rehabilitation center. It also samples institutions' ability to detect increased rates, and their capacity to respond with more aggressive hand washing campaigns, quarantine methods, and availability of yoghurt to patients at risk for infection.
==Historical Perspective==
*In 1935, Hall and O'Toole were the first to isolate ''Clostridium difficile'' from [[fecal extract]]s of healthy [[neonate]]s. Following isolation, the [[bacterium]] was originally named ''Bacillus difficilis'' because the isolation process during the original experiment was difficult.<ref name="pmid77366">{{cite journal| author=Hall IC, O’Toole E| title=Intestinal flora in new-born infants. | journal=Am J Dis Child| year= 1935 | volume= 49 | pages= 390-402}} </ref>
*The association between ''C. difficile'' and antibiotic-associated pseudomembranous colitis was first made in 1978.<ref name="pmid77366">{{cite journal| author=Larson HE, Price AB, Honour P, Borriello SP| title=Clostridium difficile and the aetiology of pseudomembranous colitis. | journal=Lancet | year= 1978 | volume= 1 | issue= 8073 | pages= 1063-6 | pmid=77366 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=77366  }} </ref><ref name="pmid700321">{{cite journal| author=Bartlett JG, Moon N, Chang TW, Taylor N, Onderdonk AB| title=Role of Clostridium difficile in antibiotic-associated pseudomembranous colitis. | journal=Gastroenterology | year= 1978 | volume= 75 | issue= 5 | pages= 778-82 | pmid=700321 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=700321  }} </ref>


It has been suggested that both the Canadian and English outbreaks were related to the seemingly more virulent 027 strain of bacterium. This strain has also been implicated in an epidemic at two Dutch hospitals (Harderwijk and Amersfoort, both 2005). A theory for explaining the increased virulence of 027 is that it is a hyperproducer of both toxin A and B, and that certain antibiotics may actually stimulate the bacteria to hyperproduce.
*[[Cell-cytotoxicity assay]] was first developed by Te-Wen Chang, who demonstrated that ''Clostridium sordellii'' antitoxin is produced among patients with pseudomembranous colitis and is able to neutralize the cytotoxic effects of an unidentified toxin (later to be identified as ''C. difficile'' toxin B).<ref name="Chang">{{cite journal| author=Chang T-W, Bartlett JG, Gorbach SL, Onderdonk AB| title=. Clindamycin induced enterocolitis in hamsters as a model of pseudomembranous colitis in patients| journal= Infect Immun| year= 1978| volume= 20 | pages= 526-9}} </ref><ref name="Barlett">{{cite journal| author=Bartlett JG, Onderdonk AB, Cisneros RL, Kasper DL| title=. Clindamycinassociated colitis due to a toxin-producing species of Clostridium in hamsters.| journal= . J Infect Dis| year= 1977| volume= 136 | pages= 701-5}} </ref>


On December 2, 2005, The New England Journal of Medicine, in an article spearheaded by Drs. Vivian Loo, Louise Poirier, and Mark Miller, reported the emergence of a new, highly toxic strain of ''C. difficile'', resistant to [[fluoroquinolone]] antibiotics, such as [[Cipro]] (ciprofloxacin) and [[Levaquin]] (levofloxacin), said to be causing geographically dispersed outbreaks in North America.<ref name=Loo_2005>{{cite journal |author=Loo V, Poirier L, Miller M, Oughton M, Libman M, Michaud S, Bourgault A, Nguyen T, Frenette C, Kelly M, Vibien A, Brassard P, Fenn S, Dewar K, Hudson T, Horn R, René P, Monczak Y, Dascal A |title=A predominantly clonal multi-institutional outbreak of Clostridium difficile-associated diarrhea with high morbidity and mortality |journal=N Engl J Med |volume=353 |issue=23 |pages=2442-9 |year=2005 |pmid=16322602}}</ref> The [[Centers for Disease Control]] in Atlanta has also warned of the emergence of an epidemic strain with increased virulence, antibiotic resistance, or both.<ref name=McDonald_2005>{{cite journal |author=McDonald L |title=''Clostridium difficile'': responding to a new threat from an old enemy |journal=Infect Control Hosp Epidemiol |volume=26 |issue=8 |pages=672-5 |year=2005 |url= http://www.cdc.gov/ncidod/dhqp/pdf/infDis/Cdiff_ICHE08_05.pdf | pmid=16156321}}</ref>
*In 2003, a [[resistant]], [[hypervirulent strain]] of ''C. difficile'' (NAP/BI/027 strain) with increased synthesis of toxins A and B was first identified. The emergence of the new strain was attributed to [[fluoroquinolone]] administration.<ref name="pmid17116920">{{cite journal| author=Bartlett JG| title=Narrative review: the new epidemic of Clostridium difficile-associated enteric disease. | journal=Ann Intern Med | year= 2006 | volume= 145 | issue= 10 | pages= 758-64 | pmid=17116920 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17116920  }} </ref><ref name="pmid16182895">{{cite journal| author=Warny M, Pepin J, Fang A, Killgore G, Thompson A, Brazier J et al.| title=Toxin production by an emerging strain of Clostridium difficile associated with outbreaks of severe disease in North America and Europe. | journal=Lancet | year= 2005 | volume= 366 | issue= 9491 | pages= 1079-84 | pmid=16182895 | doi=10.1016/S0140-6736(05)67420-X | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16182895  }} </ref><ref name="pmid16206099">{{cite journal| author=Pépin J, Saheb N, Coulombe MA, Alary ME, Corriveau MP, Authier S et al.| title=Emergence of fluoroquinolones as the predominant risk factor for Clostridium difficile-associated diarrhea: a cohort study during an epidemic in Quebec. | journal=Clin Infect Dis | year= 2005 | volume= 41 | issue= 9 | pages= 1254-60 | pmid=16206099 | doi=10.1086/496986 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16206099  }} </ref>


As one analyzes the pool of patients with the spores, many who are asymptomatic will pass the organism to individuals who are immunocompromised and hence, susceptible to increasing rates of diarrhea and poor outcome. It seems notable that the clusters described above represent a challenge to epidemiologists trying to understand how the illness spreads via the convergence of information technology with clinical surveillance.
==References==
 
On October 1, 2006, the bacteria was said to have killed at least 49 people at hospitals in Leicester, England over eight months, according to a National Health Service investigation. Another 29 similar cases were investigated by [[coroner]]s.<ref>[http://news.bbc.co.uk/1/hi/england/leicestershire/5396800.stm Trust confirms 49 superbug deaths] - [[BBC News]]</ref> A UK Department of Health memo leaked shortly afterwards revealed significant concern in government about the bacterium, described as being "endemic throughout the health service"<ref>{{cite web| url= http://www.timesonline.co.uk/article/0,,2-2541472,00.html| title=Leaked memo reveals that targets to beat MRSA will not be met| author=Nigel Hawkes| date=11th January 2007| work=The Times| accessdate = 2007-01-11}}</ref>
 
On October 27, 2006, the bacteria was attributed to 9 deaths in Quebec, Canada.<ref>{{cite web| url= http://cnews.canoe.ca/CNEWS/Canada/2006/10/27/2145519.html| title=C. difficile blamed for 9 death in hospital near Montreal| date=11th January 200| work=cNews| accessdate = 2007-01-11}}</ref>
 
On November 18th, 2006, the bacteria was reported to have been responsible for 12 deaths in Quebec, Canada. This 12th reported death was only two days after the St. Hyacinthe's Honoré Mercier announced that the outbreak was under control. 31 patients were diagnosed with Clostridium difficile and four (as of Sat. Nov 18th) were still under observation. Cleaning crews took measures in an attempt to clear the outbreak.<ref>[http://www.cbc.ca/canada/story/2006/11/18/difficile-outbreak.html 12th person dies of C. difficile at Quebec hospital] - [[CBC News]]</ref>


On February 27, 2007, a new outbreak was identified at Trillium Health Centre in Mississauga Ontario, where 14 people were diagnosed with the bacteria. The bacteria was the same strain as the one in Quebec. Officials have not been able to determine if C. difficile was responsible for deaths of four patients over the prior two months.<ref>[http://toronto.ctv.ca/servlet/an/local/CTVNews/20070228/cdifficile_mississauga_outbreak_070228/20070228/?hub=TorontoHome]</ref>
{{reflist|2}}


In October 2007, Maidstone and Tunbridge Wells NHS Trust was heavily criticized by the Healthcare Commission regarding its handling of a major outbreak of ''C. difficile'' in its hospitals in Kent from April 2004 to September 2006. In its report, the Commission estimated that about 90 patients "definitely or probably" died as a result of the infection. <ref>Healthcare Commission press release: [http://www.healthcarecommission.org.uk/newsandevents/pressreleases.cfm/cit_id/5875/FAArea1/customWidgets.content_view_1/usecache/false Healthcare watchdog finds significant failings in infection control at Maidstone and Tunbridge Wells NHS Trust], 11 October 2007</ref><ref>Daily Telegraph, [http://www.telegraph.co.uk/news/main.jhtml?xml=/news/2007/10/11/ncdiff611.xml  Health Secretary intervenes in superbug row], 11 October 2007</ref>
==References==


{{Reflist|2}}
[[Category:Infectious disease]]
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[[Category:Gastroenterology]]
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[[Category:Needs overview]]
[[Category:Bacterial diseases]]
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Latest revision as of 17:26, 18 September 2017

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yazan Daaboul, M.D.

Overview

Clostridium difficile was first isolated in 1935 during an experiment from fecal extracts of healthy neonates. The association between C. difficile and antibiotic-associated pseudomembranous colitis was first made in 1978. In 2003, a resistant, hypervirulent strain of C. difficile (NAP/BI/027 strain) with increased synthesis of toxins A and B was first identified.

Historical Perspective

  • In 1935, Hall and O'Toole were the first to isolate Clostridium difficile from fecal extracts of healthy neonates. Following isolation, the bacterium was originally named Bacillus difficilis because the isolation process during the original experiment was difficult.[1]
  • The association between C. difficile and antibiotic-associated pseudomembranous colitis was first made in 1978.[1][2]
  • Cell-cytotoxicity assay was first developed by Te-Wen Chang, who demonstrated that Clostridium sordellii antitoxin is produced among patients with pseudomembranous colitis and is able to neutralize the cytotoxic effects of an unidentified toxin (later to be identified as C. difficile toxin B).[3][4]

References

  1. ↑ 1.0 1.1 Hall IC, O’Toole E (1935). "Intestinal flora in new-born infants". Am J Dis Child. 49: 390–402.
  2. ↑ Bartlett JG, Moon N, Chang TW, Taylor N, Onderdonk AB (1978). "Role of Clostridium difficile in antibiotic-associated pseudomembranous colitis". Gastroenterology. 75 (5): 778–82. PMID 700321.
  3. ↑ Chang T-W, Bartlett JG, Gorbach SL, Onderdonk AB (1978). ". Clindamycin induced enterocolitis in hamsters as a model of pseudomembranous colitis in patients". Infect Immun. 20: 526–9.
  4. ↑ Bartlett JG, Onderdonk AB, Cisneros RL, Kasper DL (1977). ". Clindamycinassociated colitis due to a toxin-producing species of Clostridium in hamsters". . J Infect Dis. 136: 701–5.
  5. ↑ Bartlett JG (2006). "Narrative review: the new epidemic of Clostridium difficile-associated enteric disease". Ann Intern Med. 145 (10): 758–64. PMID 17116920.
  6. ↑ Warny M, Pepin J, Fang A, Killgore G, Thompson A, Brazier J; et al. (2005). "Toxin production by an emerging strain of Clostridium difficile associated with outbreaks of severe disease in North America and Europe". Lancet. 366 (9491): 1079–84. doi:10.1016/S0140-6736(05)67420-X. PMID 16182895.
  7. ↑ Pépin J, Saheb N, Coulombe MA, Alary ME, Corriveau MP, Authier S; et al. (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 (9): 1254–60. doi:10.1086/496986. PMID 16206099.
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