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Journal articles on the topic 'Clostridium difficile-associated diarrhoea'

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Published: 4 June 2021
Last updated: 12 February 2022

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1

Riley, T. V. "Clostridium difficile-associated diarrhoea." Journal of Infection 10, no. 2 (March 1985): 179–80. http://dx.doi.org/10.1016/s0163-4453(85)91753-0.

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2

Wight, N., H. Curtis, J. Hyde, S. P. Borriello, and Y. R. Mahida. "Clostridium difficile-associated diarrhoea." Postgraduate Medical Journal 74, no. 877 (November 1, 1998): 677–78. http://dx.doi.org/10.1136/pgmj.74.877.677.

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3

Elliott, B., B. J. Chang, C. L. Golledge, and T. V. Riley. "Clostridium difficile-associated diarrhoea." Internal Medicine Journal 37, no. 8 (July 19, 2007): 561–68. http://dx.doi.org/10.1111/j.1445-5994.2007.01403.x.

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4

Handler, R. "Diarrhoea associated with Clostridium difficile." Veterinary Record 120, no. 22 (May 30, 1987): 538. http://dx.doi.org/10.1136/vr.120.22.538-b.

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5

Isaacs, David. "Community-associated Clostridium difficile diarrhoea." Journal of Paediatrics and Child Health 52, no. 7 (July 2016): 783. http://dx.doi.org/10.1111/jpc.13256.

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6

V Riley, Thomas, and Clayton L Golledge. "Probiotics and Clostridium difficile-associated diarrhoea." Microbiology Australia 24, no. 1 (2003): 20. http://dx.doi.org/10.1071/ma03120.

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Clostridium difficile is now recognised as the major cause of hospital acquired infectious diarrhoea. Data from Sir Charles Gairdner Hospital (SCGH) in Perth, Western Australia, is typical of many similar hospitals in developed countries. SCGH is a 600 bed adult university teaching hospital. During the period 1983 to 1992, C. difficile was detected in 917 patients who were being investigated for diarrhoeal illness. Up to 120 patients a year were infected, most of these being elderly females. Incidence rates increased from 23/100,000 occupied bed days in 1983 to 56/100,000 occupied bed days in 1990.
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7

&NA;. "Clostridium difficile-associated diarrhoea is costly." Drugs & Therapy Perspectives 9, no. 3 (February 1997): 13–16. http://dx.doi.org/10.2165/00042310-199709030-00005.

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8

Riley, T. V., R. A. Bowman, C. F. Carson, and C. L. Golledge. "Ciprofloxacin and Clostridium difficile-associated diarrhoea." Journal of Infection 22, no. 3 (May 1991): 304–5. http://dx.doi.org/10.1016/s0163-4453(05)80023-4.

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9

Golledge, Clayton L., Christine F. Carson, Gael L. O'Neill, Rodney A. Bowman, and Thomas V. Riley. "Ciprofloxacin and Clostridium difficile-associated diarrhoea." Journal of Antimicrobial Chemotherapy 30, no. 2 (1992): 141–47. http://dx.doi.org/10.1093/jac/30.2.141.

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10

Pothoulakis, Charalabos. "Pathogenesis of Clostridium difficile-associated diarrhoea." European Journal of Gastroenterology & Hepatology 8, no. 11 (November 1996): 1041–47. http://dx.doi.org/10.1097/00042737-199611000-00003.

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11

Sclar, David Alexander, Linda M. Robison, Ambartsum M. Oganov, Jennifer M. Schmidt, Kurt A. Bowen, and Leigh V. Castillo. "Fidaxomicin for Clostridium difficile-Associated Diarrhoea." Clinical Drug Investigation 32, no. 8 (August 2012): e17-e24. http://dx.doi.org/10.1007/bf03261906.

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12

Mullish, Benjamin H., and Horace RT Williams. "Clostridium difficile infection and antibiotic-associated diarrhoea." Clinical Medicine 18, no. 3 (June 2018): 237–41. http://dx.doi.org/10.7861/clinmedicine.18-3-237.

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13

Urbina Soto, Leticia, Sara García Ávila, Ana Isabel Córdoba Alonso, M. Pía Roiz Mesones, Ana M. Arnaiz García, and M. Carmen Valero Díaz de Lamadrid. "Clostridium difficile associated diarrhoea: An increased problem." Medicina Clínica (English Edition) 147, no. 12 (December 2016): 543–46. http://dx.doi.org/10.1016/j.medcle.2016.12.043.

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14

Riley, Thomas V. "The epidemiology of Clostridium difficile-associated diarrhoea." Reviews in Medical Microbiology 5, no. 2 (April 1994): 117–22. http://dx.doi.org/10.1097/00013542-199404000-00005.

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15

Starr, John. "Clostridium difficile associated diarrhoea: diagnosis and treatment." BMJ 331, no. 7515 (September 1, 2005): 498–501. http://dx.doi.org/10.1136/bmj.331.7515.498.

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16

Al-Eidan, McElnay, Scott, and Kearney. "Clostridium difficile-associated diarrhoea in hospitalised patients." Journal of Clinical Pharmacy and Therapeutics 25, no. 2 (April 2000): 101–9. http://dx.doi.org/10.1046/j.1365-2710.2000.00266.x.

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17

Vonberg, R. P., C. Reichardt, M. Behnke, F. Schwab, S. Zindler, and P. Gastmeier. "Costs of nosocomial Clostridium difficile-associated diarrhoea." Journal of Hospital Infection 70, no. 1 (September 2008): 15–20. http://dx.doi.org/10.1016/j.jhin.2008.05.004.

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18

Aronsson, B., P. Barany, C. E. Nord, B. Nyström, and P. Stenvinkel. "Clostridium difficile-Associated diarrhoea in uremic patients." European Journal of Clinical Microbiology 6, no. 3 (June 1987): 352–56. http://dx.doi.org/10.1007/bf02017639.

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19

Surawicz, Christina M. "Probiotics, antibiotic-associated diarrhoea and Clostridium difficile diarrhoea in humans." Best Practice & Research Clinical Gastroenterology 17, no. 5 (October 2003): 775–83. http://dx.doi.org/10.1016/s1521-6918(03)00054-4.

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20

Golledge, C. L., and T. V. Riley. "Clostridium difficile-associated diarrhoea after doxycycline malaria prophylaxis." Lancet 345, no. 8961 (May 1995): 1377–78. http://dx.doi.org/10.1016/s0140-6736(95)92581-3.

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21

Chen, F., A. Chakera, C. Seow, K. Ling, A. J. Plant, and T. V. Riley. "More on Clostridium difficile -associated Diarrhoea in Australia." Anaerobe 5, no. 3-4 (June 1999): 205–7. http://dx.doi.org/10.1006/anae.1999.0202.

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22

McBride, M. O., P. J. Homer, R. I. Coker, and J. R. W. Harris. "Clostridium difficile-associated diarrhoea in HIV-infected patients." AIDS 8, no. 4 (April 1994): 557. http://dx.doi.org/10.1097/00002030-199404000-00023.

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23

Wilcox, M. H. "Clarithromycin and risk of Clostridium difficile-associated diarrhoea." Journal of Antimicrobial Chemotherapy 47, no. 3 (March 1, 2001): 358–59. http://dx.doi.org/10.1093/jac/47.3.358.

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24

Roberts, H. "Letter. Antibiotic policies and Clostridium difficile-associated diarrhoea." Age and Ageing 29, no. 4 (July 1, 2000): 369a—369. http://dx.doi.org/10.1093/ageing/29.4.369a.

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25

Vuletic, Biljana, Elizabeta Ristanovic, Slavica Markovic, Zorica Raskovic, Vladimir Radlovic, and Zoran Igrutinovic. "Clostridium difficile-associated diarrhoea in infants and children." Srpski arhiv za celokupno lekarstvo 145, no. 1-2 (2017): 85–88. http://dx.doi.org/10.2298/sarh160525018v.

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Clostridium difficile (CD) is the most common cause of nosocomial diarrhea in adults with high rates of morbidity and mortality. The epidemiology of CD infection (CDI) has changed in the last few decades associated with increasing severity of the infection rate related to the occurrence of NAP1 hypervirulent strain and the emergence of the disease among ambulatory patients and the wider community. Although little is known about CDI in pediatric patients, CD is surprisingly recognized as an important pathogen in children. In this review article, we direct attention to the recent findings on the incidence and epidemiology of pediatric CDI, including the risk factors for infection, with special emphasis on the importance of CDI in infants and a population of children suffering from chronic gastrointestinal diseases or cancer. Despite recent pharmacotherapeutic protocols successfully used in children with CDI, we would like to draw attention to precautionary and preventive measures in terms of both unnecessary testing and uncritical use of antibiotics as the most important risk factors.
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26

Halder, Kakali, Maherun Nesa, Nusrat Noor Tanni, Sharmeen Ahmed, Shaheda Anwar, Sanjida Khondakar Setu, and Ahmed Abu Saleh. "Clostridium difficile Induced Diarrhoea Among Hospitalized Patients of Tertiary Care Hospitals in Dhaka." Bangladesh Journal of Medical Microbiology 12, no. 1 (January 21, 2018): 4–9. http://dx.doi.org/10.3329/bjmm.v12i1.51684.

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Clostridium difficile (C. difficile) has become a global public health challenge as C. difficile associated-diarrhea (CDAD) is increasing in incidence and severity of disease in several countries during recent years. This cross sectional study evaluated the frequency of CDAD among 100 adult patients who were clinically diagnosed as nosocomial diarrhoea in various clinical wards of Bangabandhu Shiekh Mujib Medical University (BSMMU) and Dhaka Medical College and Hospital (DMCH). CDAD diagnosis was based on detection of C. difficile along with clinical symptoms of diarrhea. Stool microscopy was done for cytology followed by anaerobic culture in cycloserine cefoxitin fructose agar (CCFA) media, confirmed by latex agglutination of culture isolates. Toxin genes (both A and B) were detected by multiplex Polymerase chain reaction (PCR) from culture isolates. Out of 100 diarrhoeal stool samples collected, 25% samples were pus cell positive in microscopy, culture yielded growth of C. difficile in 10% samples and all isolated C. difficile were confirmed by both latex agglutination and PCR. Out of 10 isolates, 7 were only tpi (triose phosphate isomerase) gene positive which is species-specific for C. difficile indicating the presence of non-toxigenic C. difficile and 3 isolates had both tpi and toxin genes (both tcdA and tcdB gene) on PCR indicative of toxigenic C. difficile respectively. C. difficile toxin gene detection by PCR along with culture is highly specific and sensitive diagnostic modality for CDAD. Differentiation between toxigenic and non-toxigenic strains by PCR may facilitate the appropriate patient management. Bangladesh J Med Microbiol 2018; 12 (1): 4-9
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27

Gulácsi, László, Adrienne Kertész, Irén Kopcsóné Németh, János Banai, Endre Ludwig, Gyula Prinz, Péter Reményi, et al. "Clostridium difficileinfection: epidemiology, disease burden and therapy." Orvosi Hetilap 154, no. 30 (July 2013): 1188–93. http://dx.doi.org/10.1556/oh.2013.29674.

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Introduction:C. difficile causes 25 percent of the antibiotic associated infectious nosocomial diarrhoeas. C. difficile infection is a high-priority problem of public health in each country. The available literature of C. difficile infection’s epidemiology and disease burden is limited. Aim: Review of the epidemiology, including seasonality and the risk of recurrences, of the disease burden and of the therapy of C. difficile infection. Method: Review of the international and Hungarian literature in MEDLINE database using PubMed up to and including 20th of March, 2012. Results: The incidence of nosocomial C. difficile associated diarrhoea is 4.1/10 000 patient day. The seasonality of C. difficile infection is unproved. 20 percent of the patients have recurrence after metronidazole or vancomycin treatment, and each recurrence increases the chance of a further one. The cost of C. difficile infection is between 130 and 500 thousand HUF (430 € and 1665 €) in Hungary. Conclusions: The importance of C. difficile infection in public health and the associated disease burden are significant. The available data in Hungary are limited, further studies in epidemiology and health economics are required. Orv. Hetil., 2013, 154, 1188–1193.
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28

Dawson, Lisa F., Richard A. Stabler, and Brendan W. Wren. "Assessing the role of p-cresol tolerance in Clostridium difficile." Journal of Medical Microbiology 57, no. 6 (June 1, 2008): 745–49. http://dx.doi.org/10.1099/jmm.0.47744-0.

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Clostridium difficile is an important nosocomial pathogen, resulting in antibiotic-associated disease ranging from mild diarrhoea to the life-threatening pseudomembranous colitis. Upon antibiotic exposure, it is believed that the normal bowel microflora of patients is disrupted, allowing C. difficile to proliferate. Significantly, C. difficile is among only a few bacteria able to ferment tyrosine to p-cresol, a phenolic compound that is toxic to other microbes via its ability to interfere with metabolism. Therefore, the ability of different C. difficile strains to produce and tolerate p-cresol may play an important role in the development and severity of C. difficile-associated disease. In this study, it was demonstrated that two C. difficile hypervirulent 027 strains (Stoke Mandeville and BI-16) are more tolerant to p-cresol than other C. difficile strains including 630, CF4 and CD196. Surprising, it was shown that Clostridium sordellii also has a high tolerance to p-cresol, suggesting an overlap in the tolerance pathways in these clostridial species.
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29

Cunningham, R., M. Wallis, and P. Jenks. "P13.09 Testing strategy for Clostridium difficile associated diarrhoea (CDAD)." Journal of Hospital Infection 76 (October 2010): S44. http://dx.doi.org/10.1016/s0195-6701(10)60146-6.

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30

Riley, T. V., G. L. O'Neill, R. A. Bowman, and C. L. Golledge. "Clostridium difficile-associated diarrhoea: epidemiological data from Western Australia." Epidemiology and Infection 113, no. 1 (August 1994): 13–20. http://dx.doi.org/10.1017/s0950268800051414.

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SUMMARYThe incidence ofClostridium difficile-associated diarrhoea (CDAD) was investigated retrospectively at a 690-bed teaching hospital for the period 1983–92. Our aims were to determine: (i) the distribution by age and sex of patients with CDAD, (ii) the possibility of a seasonal trend and, (iii) the influence of infection control procedures, contamination of the hospital environment and the use of third-generation cephalosporins. The laboratory diagnosis of CDAD was based on demonstration of the organism by stool culture and/or detection of specific cytotoxin in stool filtrates.C. difficilewas detected in 917 patients who were being investigated for diarrhoeal illness. Yearly isolations varied from a low of 49 in 1983 to a high of 120 in 1990 (Chi square for linear trend 128·8;P <0·005). Most patients were elderly, with 63% aged 60 years or more; the majority (59%) were female. The relationship between culture ofC. difficileand detection of cytotoxin in faecal extracts was also examined. Sixty percent of a sample of 132 isolates from patients in whom faecal cytotoxin was not detected produced cytotoxinin vitro, suggesting that culture is a more sensitive indicator of infection withC. difficilethan cytotoxin detection. When the total number of faecal specimens received in the laboratory was used as a denominator there was an increase in the number of incident cases of CDAD between 1983 and 1990, apart from 1986. When occupied bed days was used as the denominator a similar trend was observed with a peak in 1990. These increases correlated with an increase in the use of third-generation cephalosporins at SCGH between 1983 and 1989 (Pearson's correlation coefficient, 0·90). The introduction of Body Substance Isolation in 1989, in conjunction with other infection control procedures, appears to have halted the rise, despite a continuing use of broad-spectrum cephalosporins. In order to reduce the number of cases of CDAD, either a reduction in levels of environmental contamination or a reduction in the use of third-generation cephalosporins is required. If this can be achieved the economic consequences, in terms of an opportunity cost, will be considerable.
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31

Paterson, David L. "Clostridium Difficile Diarrhoea Associated with Chemotherapy for Ovarian Cancer." Australian and New Zealand Journal of Obstetrics and Gynaecology 37, no. 3 (August 1997): 348–49. http://dx.doi.org/10.1111/j.1479-828x.1997.tb02428.x.

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32

Berry, A., and P. Levett. "Chronic diarrhoea in dogs associated with Clostridium difficile infection." Veterinary Record 118, no. 4 (January 25, 1986): 102–3. http://dx.doi.org/10.1136/vr.118.4.102.

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33

Gouliouris, T., D. R. Forsyth, and N. M. Brown. "Clostridium difficile-associated diarrhoea (CDAD): new and contentious issues." Age and Ageing 38, no. 5 (July 14, 2009): 497–500. http://dx.doi.org/10.1093/ageing/afp116.

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34

Greig, James. "Fidaxomicin in the Treatment of Clostridium difficile-Associated Diarrhoea." Clinical Drug Investigation 33, no. 1 (December 12, 2012): 93–94. http://dx.doi.org/10.1007/s40261-012-0044-y.

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35

Sclar, David Alexander, Linda M. Robison, Ambartsum M. Oganov, Jennifer M. Schmidt, Kurt A. Bowan, and Leigh V. Castillo. "Fidaxomicin in the Treatment of Clostridium difficile-Associated Diarrhoea." Clinical Drug Investigation 33, no. 3 (February 6, 2013): 229. http://dx.doi.org/10.1007/s40261-013-0059-z.

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36

Kato, H., H. Kato, Y. Iwashima, M. Nakamura, A. Nakamura, and R. Ueda. "Inappropriate use of loperamide worsens Clostridium difficile-associated diarrhoea." Journal of Hospital Infection 70, no. 2 (October 2008): 194–95. http://dx.doi.org/10.1016/j.jhin.2008.06.010.

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37

Macgowan, A. P., I. Brown, R. Feeney, A. Lovering, S. Y. McCulloch, D. S. Reeves, M. G. Cheesman, et al. "Clostridium difficile-associated diarrhoea and length of hospital stay." Journal of Hospital Infection 31, no. 3 (November 1995): 241–44. http://dx.doi.org/10.1016/0195-6701(95)90074-8.

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38

Shehabi, A. A., H. A. Abu Ragheb, and N. A. Allaham. "twitter sharing button linkedin sharing button facebook sharing button whatsapp sharing button email sharing button print sharing button Prevalence of Clostridium difficile-associated diarrhoea among hospitalized Jordanian patients." Eastern Mediterranean Health Journal 7, no. 4-5 (September 15, 2001): 750–55. http://dx.doi.org/10.26719/2001.7.4-5.750.

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We investigated stool specimens of 400 patients at Jordan University Hospital [300 patients with clinical diarrhoea and 100 controls without diarrhoea] for the presence of Clostridium difficile or its toxin. We found a 9.7% prevalence rate of C. difficile or its toxin in stools of patients with diarrhoea. The prevalence of other potential enteric pathogens, such as Salmonella spp. [2.3%], Shigella spp. [1.0%] and Entamoeba histolytica [2.7%], was significantly less. Prevalence of C. difficile or its toxin in controls was 3.0%. Toxin A was detected in 93.1% of C. difficile-associated diarrhoea cases using an enzyme immunoassay. Our study indicates that C. difficile-associated diarrhoea is mostly observed among hospitalized patients aged > or = 50 years, in association with antimicrobial treatment.
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39

V Riley, Thomas. "Epidemic potential and antimicrobial resistance in Clostridium difficile." Microbiology Australia 28, no. 4 (2007): 195. http://dx.doi.org/10.1071/ma07195.

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Clostridium difficile is the most commonly diagnosed cause of infectious hospital-acquired diarrhoea. C. difficile was first isolated in 1935 but not identified as the main causative agent of antibiotic-associated diarrhoea (AAD) and pseudomemranous colitis (PMC) until 1977. The spectrum of disease caused by C. difficile ranges from asymptomatic colonisation to colitis that can progress to more severe PMC. Complications include colonic perforation and death. The term C. difficile-associated diarrhoea (CDAD) is used to describe the symptomatic manifestations of the disease, thus excluding asymptomatic colonisation. Hospital inpatients with CDAD are generally elderly and have several comorbid conditions. The majority of these patients have been exposed to antimicrobials that reduce ?colonisation resistance? of the large intestine allowing subsequent infection with C. difficile. Whether infection progresses to disease is determined by many factors such as antibiotic exposure, age and comorbidities, and others that are as yet unknown. Acquisition of C. difficile is facilitated by its ability to form spores that are resistant to many disinfectants, allowing it to remain viable in the hospital environment for long periods of time. Toxigenic isolates of C. difficile usually produce two toxins, toxin A and toxin B, and these are thought of as the major virulence factors. CDAD is a major financial burden on healthcare systems, with patients spending an extra one?three weeks in hospital costing US$5?10,000 per episode.
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40

Hall, Judith, and Michael Horsley. "Diagnosis and management of patients with Clostridium difficile-associated diarrhoea." Nursing Standard 21, no. 46 (July 25, 2007): 49–56. http://dx.doi.org/10.7748/ns2007.07.21.46.49.c4589.

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41

Hove, H., M. Tvede, and P. Brøbech Mortensen. "Antibiotic-Associated Diarrhoea,Clostridium difficile, and Short-Chain Fatty Acids." Scandinavian Journal of Gastroenterology 31, no. 7 (January 1996): 688–93. http://dx.doi.org/10.3109/00365529609009151.

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42

Hall, Judith, and Michael Horsley. "Diagnosis and management of patients with clostridium difficile-associated diarrhoea." Nursing Standard 21, no. 46 (July 25, 2007): 49–60. http://dx.doi.org/10.7748/ns.21.46.49.s54.

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43

McBride, MichaelO, RichardJ Coker, PatrickJ Horner, Rosy Weston, and JonathanN Weber. "Diarrhoea associated with Clostridium difficile in AIDS patients receiving rifabutin." Lancet 343, no. 8894 (February 1994): 417. http://dx.doi.org/10.1016/s0140-6736(94)91252-1.

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44

Beaugerie, L., A. Flahault, F. Barbut, P. Atlan, V. Lalande, P. Cousin, M. Cadilhac, and J. C. Petit. "Antibiotic-associated diarrhoea and Clostridium difficile> in the community." Alimentary Pharmacology & Therapeutics 17, no. 7 (March 26, 2003): 905–12. http://dx.doi.org/10.1046/j.1365-2036.2003.01531.x.

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45

Sanderson, P. J., and S. S. Bukhari. "Candida spp. and Clostridium difficile toxin-negative antibiotic-associated diarrhoea." Journal of Hospital Infection 19, no. 2 (October 1991): 142–43. http://dx.doi.org/10.1016/0195-6701(91)90108-k.

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46

Cunney, R. "Clostridium difficile and antibiotic-associated diarrhoea - importance of C. difficile for the nephrologist." Nephrology Dialysis Transplantation 14, no. 2 (February 1, 1999): 290–92. http://dx.doi.org/10.1093/ndt/14.2.290.

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47

Numan, S. C., P. Veldkamp, E. J. Kuijper, R. J. van den Berg, and J. T. van Dissel. "Clostridium difficile-associated diarrhoea: bovine anti-Clostridium difficile whey protein to help aid the prevention of relapses." Gut 56, no. 6 (June 1, 2007): 888–89. http://dx.doi.org/10.1136/gut.2006.119016.

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48

Ludlam, H. "An antibiotic policy associated with reduced risk of Clostridium difficile-associated diarrhoea." Age and Ageing 28, no. 6 (October 1, 1999): 578–80. http://dx.doi.org/10.1093/ageing/28.6.578.

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49

Larcombe, Sarah, Melanie L. Hutton, and Dena Lyras. "Involvement of Bacteria Other Than Clostridium difficile in Antibiotic-Associated Diarrhoea." Trends in Microbiology 24, no. 6 (June 2016): 463–76. http://dx.doi.org/10.1016/j.tim.2016.02.001.

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50

Riley, T. V., J. P. Codde, and I. L. Rouse. "Increased length of hospital stay due to Clostridium difficile associated diarrhoea." Lancet 345, no. 8947 (February 1995): 455–56. http://dx.doi.org/10.1016/s0140-6736(95)90439-5.

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