as quebec strain, it has 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 toxins a and b and that certain antibiotics may stimulate the bacteria to hyperproduce. on 1 october 2006, c. difficile 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 coroners. a uk department of health memo leaked shortly afterward revealed significant concern in government about the bacterium, described as being "endemic throughout the health service" on 27 october 2006, nine deaths were attributed to the bacterium in quebec. on 18 november 2006, the bacterium was reported to have been responsible for 12 deaths in quebec. this 12th reported death was only two days after the st. hyacinthe's honoré mercier announced the outbreak was under control. thirty-one people were diagnosed with cdis. cleaning crews took measures in an attempt to clear the outbreak. c. difficile was mentioned on 6,480 death certificates in 2006 in uk. on 27 february 2007, a new outbreak was identified at trillium health centre in mississauga, ontario, where 14 people were diagnosed with cdis. the bacteria were of the same strain as the one in quebec. officials have not been able to determine whether c. difficile was responsible for the deaths of four people over the prior two months. between february and june 2007, three people at loughlinstown hospital in dublin, ireland, were found by the coroner to have died as a result of c. difficile infection. in an inquest, the coroner's court found the hospital had no designated infection control team or consultant microbiologist on staff. between june 2007 and august 2008, northern health and social care trust northern ireland, antrim area, braid valley, mid ulster hospitals were the subject of inquiry. during the inquiry, expert reviewers concluded that c. difficile was implicated in 31 of these deaths, as the underlying cause in 15, and as a contributory cause in 16. during that time, the review also noted 375 instances of cdis in those being treated at the hospital. 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 approximately 90 people "definitely or probably" died as a result of the infection. in november 2007, the 027 strain spread into several hospitals in southern finland, with 10 deaths out of 115 infected people reported on 2007-12-14. in november 2009, four deaths at our lady of lourdes hospital in ireland have possible links to cdi. a further 12 people tested positive for infection, and another 20 showed signs of infection. from february 2009 to february 2010, 199 people at herlev hospital in denmark were suspected of being infected with the 027 strain. in the first half of 2009, 29 died in hospitals in copenhagen after they were infected with the bacterium. in may 2010, a total of 138 people at four different hospitals in denmark were infected with the 027 strain plus there were some isolated occurrences at other hospitals. in may 2010, 14 fatalities were related to the bacterium in the australian state of victoria. two years later, the same strain of the bacterium was detected in new zealand. on 28 may 2011, an outbreak in ontario had been reported, with 26 fatalities as of 24 july 2011. in 2012/2013, a total of 27 people at one hospital in the south of sweden (ystad) were infected with 10 deaths. five died of the strain 017. etymology and pronunciation the genus name is from the greek klōstēr (κλωστήρ), "spindle", and the specific name is from latin difficile, neuter singular form of difficilis "difficult, obstinate", chosen in reference to fastidiousness upon culturing. regarding the pronunciation of the current and former genus assignments, clostridioides is /klɒˌstrɪdiˈɔɪdis/ and clostridium is /klɒˈstrɪdiəm/. both genera still have species assigned to them, but this species is now classified in the former. via the norms of binomial nomenclature, it is understood that the former binomial name of this species is now an alias. regarding the specific name, /dɪˈfɪsɪli/ is the traditional norm, reflecting how medical english usually pronounces naturalized new latin words (which in turn largely reflects traditional english pronunciation of latin), although a restored pronunciation of /dɪˈfɪkɪleɪ/ is also sometimes used (the classical latin pronunciation is reconstructed as ). the specific name is also commonly pronounced /ˌdiːfiˈsiːl/, as though it were french, which from a prescriptive viewpoint is a "mispronunciation" but from a linguistically descriptive viewpoint cannot be described as erroneous because it is so widely used among health care professionals; it can be described as "the non-preferred variant" from the viewpoint of sticking most regularly to new latin in binomial nomenclature, which is also a valid viewpoint, although new latin specific names contain such a wide array of extra-latin roots (including surnames and jocular references) that extra-latin pronunciation is involved anyway (as seen, for example, with ba humbugi, spongiforma squarepantsii, and hundreds of others). research as of 2019, vaccine candidates providing immunity against c. difficile toxin a and c. difficile toxin b have advanced the most in clinical research, but do not prevent bacterial colonization. a vaccine candidate by pfizer is in a phase 3 clinical trial that is estimated to be completed in september 2021 and a vaccine candidate by glaxosmithkline is in a phase 1 clinical trial that is estimated to be completed in july 2021. cda-1 and cdb-1 (also known as mdx-066/mdx-1388 and mbl-cda1/mbl-cdb1) is an investigational, monoclonal antibody combination co-developed by medarex and massachusetts biologic laboratories (mbl) to target and neutralize c. difficile toxins a and b, for the treatment of cdi. merck & co., inc. gained worldwide rights to develop and commercialize cda-1 and cdb-1 through an exclusive license agreement signed in april 2009. it is intended as an add-on therapy to one of the existing antibiotics to treat cdi. nitazoxanide is a synthetic nitrothiazolyl-salicylamide derivative indicated as an antiprotozoal agent (fda-approved for the treatment of infectious diarrhea caused by cryptosporidium parvum and giardia lamblia) and also is currently being studied in c. difficile infections vs. vancomycin. rifaximin, is a clinical-stage semisynthetic, rifamycin-based, nonsystemic antibiotic for cdi. it is fda-approved for the treatment of infectious diarrhea and is being developed by salix pharmaceuticals. other drugs for the treatment of cdi are under development and include rifalazil, tigecycline, ramoplanin, ridinilazole, and sq641. research has studied whether the appendix has any importance in c. difficile. the appendix is thought to have a function of housing good gut flora. in a study conducted in 2011, it was shown that when c. difficile bacteria were introduced into the gut, the appendix housed cells that increased the antibody response of the body. the b cells of the appendix migrate, mature, and increase the production of toxin a-specific iga and igg antibodies, leading to an increased probability of good gut flora surviving against the c. difficile bacteria. taking non-toxic types of c. difficile after an infection has promising results with respect to preventing future infections. treatment with bacteriophages directed against specific toxin-producing strains of c difficile are also being tested. a study in 2017 linked severe disease to trehalose in the diet. other animals colitis-x (in horses)