Journal articles on the topic 'Clostridium difficile (C. difficile)'

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1

Adhikari, Sushil. "Clostridium Difficile." Nepalese Medical Journal 1, no. 1 (June 22, 2018): 43–46. http://dx.doi.org/10.3126/nmj.v1i1.20400.

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Clostridium difficile ; a group of spore forming, toxin forming, gram positive anerobel is implicated in hospital associated diarrhea and is the causative agent of infectious diarrhea. It is the most common hospital associated infection in Europe and North America, and is presumed to be as prevalent in the rest of the world.There has been emergence of new virulent strain of C. difficile, identified as BI, NAP1, and toxinotype III and ribotype 027 (subsequently known as BI/NAP1/027) by various typing method in recent years, implicated in dramatic increase in C. difficile infections.Diagnosis is established by presence of C. difficile toxin or C. difficile toxin gene in stool. Lab testing does not distinguish C. difficile infection and asymptomatic carriage. Clinical suspicion and positive stool study confirms a diagnosis.Clostridium Difficile infection, is most common health care associated infection in Europe and North America, and the available studies show it may have similar prevalence in Nepal. Literature review does not reveal any significant study being conducted in Nepal as of now. It warrants further study to exactly determine the incidence/prevalence and its impact in current health care in Nepal. Clinicians need increased awareness and prompt diagnosis to reduce morbidity and further prevention of transmission.Nepalese Medical Journal, vol.1, No. 1, 2018, page: 43-47
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2

Johnson, S. "Clostridium difficile Toxins and Severe C. difficile Infection." Journal of Infectious Diseases 205, no. 3 (December 5, 2011): 353–54. http://dx.doi.org/10.1093/infdis/jir752.

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3

Hossain, M., TJ Crook, and SR Keoghane. "Clostridium Difficile in Urology." Annals of The Royal College of Surgeons of England 90, no. 1 (January 2008): 36–39. http://dx.doi.org/10.1308/003588408x242358.

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INTRODUCTION The objective was to determine the incidence of Clostridium difficile infection in a UK urology ward from 2000 to 2005, and correlate and compare the data with other specialty wards and national figures. PATIENTS AND METHODS Urology patients with a positive stool culture for C. difficile between 2000 and 2005 were identified from a hospital database. The medical records of these patients were reviewed and data such as antibiotic use, urological diagnosis and elective/emergency status of the patient were recorded and analysed. The number of C. difficile cases on an elderly care ward, an acute medical ward and an acute surgical ward were also recorded for this period. Data on the number of admissions and occupied bed-days on all 4 wards were compared. RESULTS There were 33 cases of C. difficile on the urology ward between 2000 and 2005. The incidence of this infection varied between 10.2 and 48.4 cases per 10,000 patient episodes (mean 21.0). There was a significant difference between the number of C. difficile cases per 1000 patient days between the urology ward and the acute medical ward (P = 0.002) and the elderly care ward (P = 0.03). CONCLUSIONS There is no evidence to suggest that there has been an increase in the incidence of C. difficile in a UK urology ward. The rates on the urology ward were lower than the national average, and significantly lower than those rates on an acute medical ward and an elderly care ward. There is a 0.21% chance of a patient testing positive for C. difficile during their stay on a urology ward.
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Itoh, K., W. K. Lee, H. Kawamura, T. Mitsuoka, and T. Magaribuchi. "Intestinal bacteria antagonistic to Clostridium difficile in mice." Laboratory Animals 21, no. 1 (January 1, 1987): 20–25. http://dx.doi.org/10.1258/002367787780740662.

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Overgrowth by Clostridium difficile has been reported in conventional mice injected intraperitoneally with ampicillin. In this study, we aimed to determine which types of indigenous intestinal bacteria were eliminated by ampicillin to allow overgrowth by C. difficile C. difficile overgrowth was associated with a decrease in the numbers of lactobacilli, an increase in bacteroidaceae and a slight decrease in the frequency of isolation of fusiform-shaped bacteria (clostridia). C. difficile cytotoxin was detected in caeca from mice in which the numbers of C. difficile were greater than 105 per gram of faeces. Gnotobiotic mice were inoculated with various groups of intestinal anaerobes to determine which members of the indigenous flora would antagonize C. difficile. Gnotobiotic mice inoculated with three strains of lactobacilli, 37 strains of bacteroides or 46 strains of clostridia isolated from limited-flora mice were unable to eliminate C. difficile. C. difficile was eliminated, however, from the gastrointestinal tracts of gnotobiotic mice inoculated with whole faeces or chloroform-treated faeces from conventional mice or whole faeces from limited-flora mice containing only clostridia.
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5

Stein, R. B. "Clostridium difficile Toxoid Vaccine in Recurrent C. difficile–Associated Diarrhea." Yearbook of Gastroenterology 2006 (January 2006): 177–78. http://dx.doi.org/10.1016/s0739-5930(08)70370-2.

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6

Sougioultzis, Stavros, Lorraine Kyne, Denise Drudy, Sarah Keates, Seema Maroo, Charalabos Pothoulakis, Paul J. Giannasca, et al. "Clostridium difficile toxoid vaccine in recurrent C. difficile-associated diarrhea." Gastroenterology 128, no. 3 (March 2005): 764–70. http://dx.doi.org/10.1053/j.gastro.2004.11.004.

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7

Mohamed, Abdalla, Vanessa Sostre, Hiren Patel, Prem Patel, Luis C. Ortiz, and Walid J. Baddoura. "Clostridium difficile Causing Empyema." Case Reports in Gastroenterology 12, no. 3 (October 24, 2018): 633–39. http://dx.doi.org/10.1159/000493184.

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Extraintestinal Clostridium difficile infection (CDI) is extremely uncommon. High mortality and poor outcomes have been observed among individuals with this rare medical condition. Empyema is one of the extraintestinal manifestations of CDI. Possible mechanisms to develop this parapneumonic effusion are aspiration and contamination of the chest tube. We present a 42-year-old Hispanic male with C. difficile empyema without any prior history of CDI.
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8

Androga, Grace O., Alan M. McGovern, Briony Elliott, Barbara J. Chang, Timothy T. Perkins, Niki F. Foster, and Thomas V. Riley. "Evaluation of the Cepheid Xpert C. difficile/Epiand Meridian Bioscienceillumigene C. difficile Assays for Detecting Clostridium difficile Ribotype 033 Strains." Journal of Clinical Microbiology 53, no. 3 (December 17, 2014): 973–75. http://dx.doi.org/10.1128/jcm.03297-14.

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Clostridium difficilePCR ribotype 033 (RT033) is found in the gastrointestinal tracts of production animals and, occasionally, humans. TheillumigeneC. difficileassay (Meridian Bioscience, Inc.) failed to detect any of 52C. difficileRT033 isolates, while all strains signaled positive for the binary toxin genes but were reported as negative forC. difficileby the XpertC. difficile/Epiassay (Cepheid).
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9

Sanghi, P., A. Oates, and A. K. Scott. "Antibiotic Policy and Clostridium Difficile." Age and Ageing 24, suppl 1 (January 1, 1995): P27—P28. http://dx.doi.org/10.1093/ageing/24.suppl_1.p27-c.

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10

Bartlett, John G. "Detection of Clostridium difficile Infection." Infection Control & Hospital Epidemiology 31, S1 (November 2010): S35—S37. http://dx.doi.org/10.1086/655999.

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There has been a recent surge of interest in Clostridium difficile infection, which reflects an impressive increase in the number and severity of these infections. This review addresses some of the newer methods for detection of C. difficile infection at the bedside and in the laboratory. Particularly important are the new rapid diagnostic tests that detect toxigenic C. difficile using polymerase chain reaction and the combination tests that, either simultaneously or sequentially, screen for C. difficile and test for toxins A and B. It is expected that these new testing methods will largely supplant the enzyme immunoassays for toxins, which are used by most laboratories, departments, and divisions. The present goal is to combine clinical, laboratory, and animal research related to C. difficile that reflects issues that are considered to be major contemporary challenges. Among this work is the pursuit of studies of immune mechanisms to better control this disease.
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11

Causey, M. Wayne, Michael P. Spencer, and Scott R. Steele. "Clostridium difficile Enteritis after Colectomy." American Surgeon 75, no. 12 (December 2009): 1203–6. http://dx.doi.org/10.1177/000313480907501211.

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Clostridium difficile infection of the colon is, unfortunately, a relatively common occurrence that typically follows treatment with antibiotics; however, C. difficile infection of the small bowel is a much more rare phenomenon with only 19 cases reported to date. We present three cases of isolated C. difficile enteritis after colectomy. Although all three patients were identified early and successfully treated with medical management without the need for surgical intervention, previous authors have suggested a much higher morbidity and mortality rate with this infection. This article reviews the current available literature on C. difficile enteritis to highlight this potentially serious condition in postoperative colectomy patients who present with low-grade fevers, abdominal or pelvic pain, and increased ileostomy output.
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12

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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13

Bobulsky, G. S., W. N. Al-Nassir, M. M. Riggs, A. K. Sethi, and C. J. Donskey. "Clostridium difficile Skin Contamination in Patients with C. difficile-Associated Disease." Clinical Infectious Diseases 46, no. 3 (February 1, 2008): 447–50. http://dx.doi.org/10.1086/525267.

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14

Pancholi, P., C. Kelly, M. Raczkowski, and J. M. Balada-Llasat. "Detection of Toxigenic Clostridium difficile: Comparison of the Cell Culture Neutralization, Xpert C. difficile, Xpert C. difficile/Epi, and Illumigene C. difficile Assays." Journal of Clinical Microbiology 50, no. 4 (January 25, 2012): 1331–35. http://dx.doi.org/10.1128/jcm.06597-11.

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15

Silva Júnior, Moacyr. "Recent changes in Clostridium difficile infection." Einstein (São Paulo) 10, no. 1 (March 2012): 105–9. http://dx.doi.org/10.1590/s1679-45082012000100023.

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Clostridium difficile is the main cause of nosocomial diarrhea. Diarrhea associated with C. difficile has increased incidence, morbidity, and mortality in the last few years. The major related risk factors include use of antibiotics, elderly patients and prolonged hospital stay. Many patients receive combinations of antibiotics or multiple antibiotics, which represents the main risk to develop diarrhea associated to C. difficile or its recurrence. Therefore, interventions to improve antibiotic prescribing, as well as compliance with infection control measures can reduce hospital-acquired C. difficile infections. This review addresses the epidemiological changes in C. difficile disease and its treatment.
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16

George Trad, Varun Sodhi, Matthew Brockway, Nazanin Sheikhan, Abdul Gader Gheriani, Olivia Astor, and Hatim Gemil. "Clostridioides (Clostridium) difficile infection: Review of literature." World Journal of Advanced Research and Reviews 14, no. 2 (May 30, 2022): 146–55. http://dx.doi.org/10.30574/wjarr.2022.14.2.0366.

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Clostridioides (Clostridium) difficile (C. difficile) is a gram-positive bacterium that infects the large intestine. The number of clostridium difficile infections has increased in the recent years due to multiple risk factors including frequent use of antibiotics and proton pump inhibitors. The virulence of C. difficile comes from its production of toxins. Treatment for C. difficile infection includes the use of antibiotics, monoclonal antibodies, or a fecal transplant.
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17

Telekes, András. "A Clostridium difficile onkológiai vonatkozásai." Orvosi Hetilap 157, no. 28 (July 2016): 1110–16. http://dx.doi.org/10.1556/650.2016.30463.

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Clostridium difficile infection is one of the most frequent among cancer patients. Its diagnosis is complicated by the fact that the symptoms of the infection and the side effects of the anticancer treatments could be similar. Chemotherapy itself might facilitate Clostridium difficile infection. Several risk factors are known but Clostridium difficile infection can develop in the absence of these. Neutreopenia is a risk factor for fatal Clostridium difficile infection and also the side effect of chemotherapy. Therefore, if symptoms of the potential infection develop (eg. diarrhoea more than three times a day, fever above 38.5 °C, colitis, rapid increase of serum creatinin) Clostridium difficile infection should be excluded. If the infection is confirmed it should be managed in the most efficient way. Orv. Hetil., 2016, 157(28), 1110–1116.
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18

NIKOLAEVA, I. V., S. V. KHALIULLINA, G. Kh MURTAZINA, and V. A. ANOKHIN. "Clostridioides (Clostridium) difficile infection. Review of current clinical guidelines." Practical medicine 18, no. 6 (2020): 106–12. http://dx.doi.org/10.32000/2072-1757-2020-6-106-112.

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Clostridioides difficile (CDI) infection is a disease associated with a disruption of the gut microbiome with over-colonization of C. difficile, the toxins of which cause inflammation and damage to the colon. A dynamic assessment of the CDI prevalence indicates a significant increase in laboratory-confirmed cases of infection and a high mortality associated with it. C. difficile is recognized as the main causative agent of nosocomial infections in Europe, USA, Canada and Australia, which develops 48 hours after hospitalization in a medical facility and within 12 weeks after discharge. The severity of CDI is determined by the severity of infectious-toxic, diarrheal and abdominal syndromes. Severe CDI is characterized by manifestations of colitis, accompanied by severe leukocytosis, a decrease in albumin levels and an increase in serum creatinine levels. Development of fulminant forms, pseudomembranous colitis, toxic megacolon, intestinal perforation, sepsis is possible. The risk factors include in-hospital stay; recent use of antibiotics (within the previous 12 weeks, especially the use of fluoroquinolones, cephalosporins of III–IV generations, carbapenems and clindamycin), PPI and H2-histamine blockers; presence of inflammatory bowel diseases (ulcerative colitis, Crohn’s disease), immunodeficiency states, including iatrogenic; recent endoscopic examinations, surgical interventions on the gastrointestinal tract, tube feeding, enemas; possible contact with a family member who recently had a C..difficile infection. The «gold standard» for confirming the CDI diagnosis is the identification of the causative agent and/or toxins of C. difficile in the stool using specific laboratory research methods. Vancomycin or metronidazole are recommended as first-line therapy.
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19

Sorg, Joseph A., and Abraham L. Sonenshein. "Bile Salts and Glycine as Cogerminants for Clostridium difficile Spores." Journal of Bacteriology 190, no. 7 (February 1, 2008): 2505–12. http://dx.doi.org/10.1128/jb.01765-07.

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ABSTRACT Spore formation by Clostridium difficile is a significant obstacle to overcoming hospital-acquired C. difficile-associated disease. Spores are resistant to heat, radiation, chemicals, and antibiotics, making a contaminated environment difficult to clean. To cause disease, however, spores must germinate and grow out as vegetative cells. The germination of C. difficile spores has not been examined in detail. In an effort to understand the germination of C. difficile spores, we characterized the response of C. difficile spores to bile. We found that cholate derivatives and the amino acid glycine act as cogerminants. Deoxycholate, a metabolite of cholate produced by the normal intestinal flora, also induced germination of C. difficile spores but prevented the growth of vegetative C. difficile. A model of resistance to C. difficile colonization mediated by the normal bacterial flora is proposed.
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20

Vaishnavi, Chetana. "Decontamination Strategies for Control of Environmental Clostridium difficile (Decontamination and C. difficile)." Global Journal of Pathology and Microbiology 2, no. 1 (June 2014): 22–34. http://dx.doi.org/10.14205/2310-8703.2014.02.01.4.

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21

Zhou, Yuan, Larissa Lewis, Michelle McIntosh, Ferric C. Fang, Ronald Pergamit, Timothy Dellit, and John B. Lynch. "Risk factors for Clostridium difficile infection in C. difficile colonized ICU patients." Open Forum Infectious Diseases 4, suppl_1 (2017): S403. http://dx.doi.org/10.1093/ofid/ofx163.1007.

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Abstract Background Clostridium difficile is a major cause of healthcare-associated infections leading to significant morbidity and mortality; however, data-driven interventions to decrease C. difficile infections (CDI) are lacking due to an incomplete understanding of disease transmission and risk factors. Asymptomatic C. difficile carriers may be an important source of nosocomial transmission and disease but few studies have examined colonized patients who later develop CDI. We describe risk factors for the development of CDI in a critical care population screened for C. difficile colonization. Methods All patients admitted to our medical or trauma ICUs were screened for toxigenic C. difficile by PCR via rectal swab. Colonized patients were placed in contact enteric precautions for their entire hospitalization and monitored for signs and symptoms of CDI. Retrospective chart review assessed risk factors associated with development of CDI. Results 868 rectal swabs were collected from 4/01/16 to 10/31/16. 40 patients were colonized with C. difficile on ICU admission and 20 developed symptomatic CDI (Table 1). Risk factors for CDI in colonized patients include enteral feeding and exposure to antibiotics (Table 2). Conclusion 50% of C. difficile colonized ICU patients progressed to symptomatic CDI during their hospitalization. Antibiotic use was a significant risk factor for CDI. C. difficile carriers may be a particularly vulnerable population for CDI, warranting further investigation for early identification of colonized patients and strategies for infection prevention. Disclosures F. C. Fang, BioFire: Collaborator, Consultant and Scientific Advisor, Consulting fee, Research support and Speaker honorarium; Cepheid: Collaborator, Consultant and Scientific Advisor, Consulting fee, Educational grant, Research support and Speaker honorarium
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Murillo, J., V. Heitzer, M. Ruiz, and F. Ordieres. "Initiatives to decrease the incidence and transmission of Clostridium difficile (C. difficile)." International Journal of Infectious Diseases 14 (March 2010): e251-e252. http://dx.doi.org/10.1016/j.ijid.2010.02.2048.

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23

Adukauskienė, Dalia, Justina Čyžiūtė, Rytis Mickus, and Asta Dambrauskienė. "DĖMESIO: CLOSTRIDIUM DIFFICILE INFEKCIJA." Visuomenės sveikata 29, no. 2 (April 27, 2019): 28–34. http://dx.doi.org/10.5200/sm-hs.2019.013.

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Nors Clostridium difficile infekcijos (CDI) protrūkis pasaulyje stebėtas daugiau nei prieš dešimtmetį, sergamumas ja tebėra itin didelis, ir ji išlieka aktuali hospitalinė problema. Šio tyrimo tikslas – nustatyti Clostridium difficile infekcijos dinamiką per penkerius metus bei palyginti žinomų šios infekcijos rizikos veiksnių dažnį, klinikinės eigos ypatybes ir baigtis 2011 m. ir 2015 m. pacientų imtyse. Atlikta retrospektyvi ligos istorijų duomenų analizė pacientų ≥ 18 m., gydytų Lietuvos sveikatos mokslų universiteto ligoninės Kauno klinikose 2011 m. ir 2015 m., kuriems kliniškai pasireiškė diarėja (≥ nei 3 pasituštinimai per dieną ir/ar padaugėjęs išmatų kiekis > 200 g per dieną) bei rastas C. difficile A ir/ ar B toksinas išmatose. Statistinė duomenų analizė atlikta naudojant kompiuterinę programą SPSS 23,0. Hipotezių tikrinimui taikytas α = 0,05 reikšmingumo lygmuo. Tyrimui atlikti gautas Bioetikos komiteto leidimas Nr. (BEC-MF-869). Į galutinę duomenų analizę įtraukti septyni 2011 m. ir septyniasdešimt du 2015 m. pacientai. Skirtumų tarp 2011 m. ir 2015 m. grupių pagal amžių ir lytį nenustatyta (p > 0,05). 2015 m. amžiaus grupėje ≥ 65 m. buvo n=45 (62,5%) pacientai, (p = 0,045). 2011 m. terapijos skyriuose buvo diagnozuoti n=5 (71,4%) CDI atvejai ir po n=1 (14,3%) atvejį chirurgijos ir intensyviosios terapijos skyriuose. 2015 m. n=60 (83,3%) CDI atvejų buvo diagnozuoti terapijos skyriuose, o n=12 (16,7%) atvejų – chirurgijos skyriuose, (p = 0,01). Antibiotikus iki CDI išsivystymo 2011 m. vartojo visi, 2015 m. – n=69 (95,8%) pacientai (p > 0,05). Antros kartos cefalosporiną (cefuroksimą) iki CDI išsivystymo buvo vartoję n=7 (100%), 2015 m. – n=56 (81,2 %) pacientai (p > 0,05). Skirtumų pagal rizikos veiksnių pasireiškimą tarp 2011 m. ir 2015 m. grupių nenustatyta (p > 0,05). Sunki būklė (Charlson Comorbidity Index ≥ 5 balai) 2011 m. nustatyta n=6 (85,7%), 2015 m. n=46 (63,9%) pacientams, (p = 0,025). Skirtumų pagal Charlson Comorbidity Index tarp 2011 m. ir 2015 m. grupių nenustatyta (p > 0,05). Visi 2011 m. CDI atvejai n=7 (100%) buvo hospitalinė CDI; 2015 m. jų buvo n=60 (83,3%), su sveikatos priežiūra susijusios CDI – n=11 (15,3%) ir visuomenėje įgytos CDI – n=1 (1,4%) atvejis, (p = 0,01). Rekurentinė CDI 2011 m. nenustatyta, 2015 m. išsivystė n=6 (8,3%) pacientams (p > 0,05). Dėl CDI į intensyviosios terapijos skyrių 2011 m. buvo hospitalizuotas n=1 (14,3%), 2015 m. – n=4 (5,6%) pacientai, visi jie mirė, kaip ir mirė 2011 m. vienas pacientas, kuriam CDI išsivystė intensyviosios terapijos skyriuje. Tiriamuoju laikotarpiu Clostridium difficile infekcijos padaugėjo 10 kartų. 2011 m. ir 2015 m. pacientų grupės pagal demografinę charakteristiką buvo homogeniškos, o 2015 m. dažniau ja sirgo pagyvenę pacientai ir dažniausiai išsivystė terapijos skyriaus pacientams. Dažniausias infekcijos rizikos veiksnys abiejose grupėse buvo antibiotikų vartojimas, antrasis pagal dažnumą – imunosupresinė būklė. Dažniausiai vartotas antibiotikas, kurio fone išsivystė Clostridium difficile infekcija, buvo cefuroksimas. Šalutinių ligų indeksas (Charlson Comorbidity Index) nurodė, kad 2015 m. padažnėjus infekcijai vyravo sunkios būklės dėl šalutinių susirgimų pacientai. Trys penktadaliai Clostridium difficile infekcijos atvejų 2015 m. buvo hospitalinės kilmės. Daugėjo rekurentinės eigos infekcijų, nors dėl imties aspektų statistinio patikimumo negauta. Komplikacija – stacionarizavimas į intensyviosios terapijos skyrių dėl Clostridium difficile infekcijos buvo susijęs su jau kritinės būklės pacientų mirtimi.
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Kwon, Jennie H., Tiffany Hink, Kimberly Reske, Erik R. Dubberke, and Carey-Ann D. Burnham. "Etiology of Infectious Diarrhea in Patients Tested for Clostridium difficile: If It Isn’t Clostridium difficile, What Is It?" Open Forum Infectious Diseases 4, suppl_1 (2017): S2. http://dx.doi.org/10.1093/ofid/ofx162.004.

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Abstract Background The objective of the study was to assay for alternative infectious causes of diarrhea in patients with negative EIA tests for Clostridium difficile. Methods A hard-stop alert was implemented at a tertiary care hospital to limit repeat testing for C. difficile within 96 hours of an initial negative EIA. Stool samples from patients with a negative (–) repeat EIA test for C. difficile within 96 hours in the 3 months pre- and postintervention underwent further evaluation: C. difficile toxigenic culture, GeneXpert C. difficile PCR, Biofire Gastrointestinal (GI) Panel, and culture on a blood agar plate. Results Of the 84 C. difficile EIA stool specimens evaluated, 8% were toxigenic culture positive (+), 8% tested + for C. difficile via the Biofire GI panel, and 5 (7%) + with the GenXpert C. difficile PCR (Table 1). Three of these patients were diagnosed with CDI within 30 days of a + test. Five patients were + for Norovirus via Biofire GI panel; none were tested for or diagnosed with Norovirus. Two patients were + for Enteropathogenic E. coli and one for Enteroaggregative E. coli via Biofire GI panel; none were tested for or diagnosed with E. coli infection. One patient was positive for Salmonella and Salmonella was isolated by stool culture. Conclusion Patients tested for C. difficile may have alternate causes of diarrhea. When evaluating hospitalized patients with diarrhea, C. difficile, along with alternate causes of diarrhea can be considered. Disclosures E. R. Dubberke, Merck: Consultant, Consulting fee; Biofire: one time talk, Speaker honorarium;; Alere: one-time talk, Speaker honorarium; Sanofi pasteur: Grant Investigator, Grant recipient; Pfizer: Consultant, Consulting fee; Rebiotix: Investigator, Research support; Rebiotix: Consultant, Consulting fee; valneva: Consultant, Consulting fee; C. A. D. Burnham, bioMerieux: Grant Investigator, Research grant; ThermoFisher: Consultant, Salary; Cepheid: Grant Investigator, Research grant
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FAWLEY, W. N., and M. H. WILCOX. "Molecular epidemiology of endemic Clostridium difficile infection." Epidemiology and Infection 126, no. 3 (June 2001): 343–50. http://dx.doi.org/10.1017/s095026880100557x.

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This is the first study to provide a comprehensive insight into the molecular epidemiology of endemic Clostridium difficile and particularly that associated with a recently recognized epidemic strain. We DNA fingerprinted all C. difficile isolates from the stools of patients with symptomatic antibiotic-associated diarrhoea and from repeated samples of the inanimate ward environment on two elderly medicine hospital wards over a 22-month period. Notably, C. difficile was not recoverable from either ward immediately before opening, but was found on both wards within 1–3 weeks of opening, and the level of environmental contamination rose markedly during the first 6 months of the study period. C. difficile infection (CDI) incidence data correlated significantly with the prevalence of environmental C. difficile on ward B (r = 0·76, P < 0·05) but not on ward A (r = 0·26, P > 0·05). We found that RAPD and RS–PCR typing had similar discriminatory power, although, despite fingerprinting over 200 C. difficile isolates, we identified only six distinct types. Only two distinct C. difficile strains were identified as causing both patient infection and ward contamination. Attempts to determine whether infected patients or contaminated environments are the prime source for cross-infection by C. difficile had limited success, as over 90% of C. difficile isolates were the UK epidemic clone. However, a non-epidemic strain caused a cluster of six cases of CDI, but was only isolated from the environment after the sixth patient became symptomatic. The initial absence of this strain from the environment implies patient-to-patient and/or staff-to-patient spread. In general, routine cleaning with detergent was unsuccessful at removing C. difficile from the environment. Understanding the epidemiology and virulence of prevalent strains is important if CDI is to be successfully controlled.
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Hui, Liangliang, Kui Zang, Min Wang, Futai Shang, and Guoxin Zhang. "Coculture with Clostridium difficile promotes apoptosis of human intestinal microvascular endothelial cells." Journal of International Medical Research 46, no. 11 (November 2018): 4731–39. http://dx.doi.org/10.1177/0300060518799267.

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Objective The clostridial triose-phosphate isomerase ( tpi) gene is a housekeeping gene that specifically distinguishes Clostridium difficile from other bacteria. This retrospective cohort study was performed to analyze and compare the TPI protein-positive rates in outpatients and hospitalized patients with and without diarrhea (control group). Methods Western blotting, methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay, and flow cytometry were used to investigate the pathogenic mechanism of C. difficile in the development and progression of diarrhea in patients with inflammatory bowel disease (IBD). Results The TPI protein-positive rates were significantly higher in patients with diarrhea but without IBD than in the healthy control group as well as in patients with diarrhea and IBD than in patients with diarrhea but without IBD. Coculture with C. difficile inhibited aquaporin-1 protein expression in human intestinal microvascular endothelial cells, which significantly reduced the proliferation of these cells and promoted their apoptosis. Conclusions Clostridium difficile infection is associated with diarrhea and may be an important risk factor for diarrhea in patients with IBD. Coculture with C. difficile may inhibit the proliferation of intestinal mucosal cells and promote their apoptosis, reduce intestinal aquaporin-1 expression, and inhibit intestinal water uptake. Clostridium difficile is one cause of C. difficile-associated diarrhea.
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Lawley, Trevor D., Nicholas J. Croucher, Lu Yu, Simon Clare, Mohammed Sebaihia, David Goulding, Derek J. Pickard, Julian Parkhill, Jyoti Choudhary, and Gordon Dougan. "Proteomic and Genomic Characterization of Highly Infectious Clostridium difficile 630 Spores." Journal of Bacteriology 191, no. 17 (June 19, 2009): 5377–86. http://dx.doi.org/10.1128/jb.00597-09.

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ABSTRACT Clostridium difficile, a major cause of antibiotic-associated diarrhea, produces highly resistant spores that contaminate hospital environments and facilitate efficient disease transmission. We purified C. difficile spores using a novel method and show that they exhibit significant resistance to harsh physical or chemical treatments and are also highly infectious, with <7 environmental spores per cm2 reproducibly establishing a persistent infection in exposed mice. Mass spectrometric analysis identified ∼336 spore-associated polypeptides, with a significant proportion linked to translation, sporulation/germination, and protein stabilization/degradation. In addition, proteins from several distinct metabolic pathways associated with energy production were identified. Comparison of the C. difficile spore proteome to those of other clostridial species defined 88 proteins as the clostridial spore “core” and 29 proteins as C. difficile spore specific, including proteins that could contribute to spore-host interactions. Thus, our results provide the first molecular definition of C. difficile spores, opening up new opportunities for the development of diagnostic and therapeutic approaches.
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Prechter, Florian, and Andreas Stallmach. "Clostridium difficile auf der Intensivstation." Wiener klinisches Magazin 23, no. 5 (August 18, 2020): 210–17. http://dx.doi.org/10.1007/s00740-020-00354-0.

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Zusammenfassung Auf der Intensivstation ist die Clostridienenteritis mit einer Prävalenz von 1–2 % der Patienten eine nicht seltene Erkrankung, die den Behandler vor besondere Herausforderungen stellt. Für Europa liegen nur wenige belastbare Daten bezüglich Schweregrad und Therapie der Clostridium difficile Infektionen (CDI) bei Intensivpatienten vor; die Übertragbarkeit von Ergebnissen aus Studien mit anderen Patientenkollektiven ist teilweise problematisch. Auch die Empfehlungen zu Diagnostik und Therapie sind auf diese Patienten aufgrund der meist ausgeprägten Komorbiditäten oft nur mit Einschränkungen anwendbar. Zudem zeigt sich in letzter Zeit immer deutlicher, dass bei einem mit 10–20 % relevanten Teil aller Patienten eine asymptomatische Kolonisation mit C. difficile besteht, die in ihrer Relevanz für den Patienten und für die Übertragung im Krankenhaus bislang nicht gut verstanden ist. Unter Berücksichtigung der aktuellen Literatur geben wir einen Überblick über aktuelle Herausforderungen in Diagnostik und Verlaufsabschätzung, primäre Behandlungsoptionen sowie Behandlungsalternativen bei besonderen Problemen und Therapieversagen. Zudem gehen wir auf die Prävention von Neuerkrankungen auf der Intensivstation ein.
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Mizrahi, Hamo, Azrad, and Peretz. "Molecular Characterization and Moxifloxacin Susceptibility of Clostridium difficile." Antibiotics 8, no. 3 (August 12, 2019): 118. http://dx.doi.org/10.3390/antibiotics8030118.

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In recent years, the incidence and severity of Clostridium difficile infections has increased.Additionally, resistance of C. difficile to frequently used antibiotics is rising. To improve ourunderstanding of C. difficile, there is a need for molecular characterization of different strains andantibiotic resistance testing. We investigated the efficacy of GenoType CDiff kit (Hain Lifesciences)in identification of C. difficile and its various strains in northern Israel. The kit involves a molecularassay that detects C. difficile from stool samples or colonies and identifies the different strains andmutations in the gyrA gene that cause moxifloxacin resistance. Forty‐nine C. difficile positive sampleswere examined by the kit following DNA extraction from both colonies and stool. The identificationrate (95.9%) of C. difficile was much higher when DNA was extracted from colonies, compared toextraction from stool (46.9%). Low frequencies of ribotype027 strain (2%) and of ribotype078 strain(4%) were found. There was a high concordance between genotype (mutation in gyrA) andphenotype (Etest) for moxifloxacin resistance (Kappa=0.72). A high percentage of moxifloxacinresistantstrains was found. Our findings indicate that the GenoType CDiff kit is very effective incharacterization of C. difficile strains and less effective for identification of C. difficile directly fromstool samples.
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Squire, Michelle M., and Thomas V. Riley. "Clostridium difficile infection: the next big thing!" Microbiology Australia 33, no. 4 (2012): 163. http://dx.doi.org/10.1071/ma12163.

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Clostridium difficile causes infectious diarrhoea in humans and animals. It has been found in pigs, horses, and cattle, suggesting a potential reservoir for human infection, and in 20-40% of meat products in Canada and the USA, suggesting the possibility of food-borne transmission. It is likely that excessive antimicrobial exposure is driving the establishment of C. difficile in animals, in a manner analogous to human infection, rather than the organism just being normal flora of the animal gastrointestinal tract. Outside Australia, PCR ribotype 078 is the most common ribotype of C. difficile found in pigs (83% in one study in the USA) and cattle (up to 100%) and this ribotype is now the third most common ribotype of C. difficile found in humans in Europe. Human and pig strains of C. difficile are genetically identical in Europe confirming that a zoonosis exists. Rates of community-acquired C. difficile infection (CDI) are increasing world-wide, and a new community strain of unidentified origin has recently emerged in Australia. Environmental contamination may also play a role. C. difficile spores survive in treated piggery effluent, the by-products of which are used to irrigate crops and pasture and manufacture compost. There is abundant evidence that food products intended for human consumption contain toxigenic strains of C. difficile but food-borne transmission remains unproven. Thus there are four problems that require resolution: a human health issue, an animal health issue and the factors common to both these problems, environmental contamination and antimicrobial misuse.
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Weese, J. Scott. "Clostridium (Clostridioides) difficile in animals." Journal of Veterinary Diagnostic Investigation 32, no. 2 (January 6, 2020): 213–21. http://dx.doi.org/10.1177/1040638719899081.

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Clostridium ( Clostridioides) difficile is a gram-positive, spore-forming bacterium that is an important cause of disease in people, a variably important cause of disease in some animal species, and an apparently harmless commensal in others. Regardless of whether it is a known pathogen in a particular species, it can also be found in healthy individuals, sometimes at high prevalences and typically with higher rates of carriage in young individuals. As it is investigated in more animal species, it is apparent that this bacterium is widely disseminated in a diverse range of domestic and wild animal species. Although it can be found in most species in which investigations have been performed, there are pronounced intra- and inter-species differences in prevalence and clinical relevance. A wide range of strains can be identified, some that appear to be animal associated and others that are found in humans and animals. A large percentage of strains that cause disease in people can at least sporadically be found in animals. It is a potentially important zoonotic pathogen, but there is limited direct evidence of animal–human transmission. Although C. difficile has been studied extensively over the past few decades, it remains an enigmatic organism in many ways.
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Gilbreath, Jeremy J., Punam Verma, April N. Abbott, and Susan M. Butler-Wu. "Comparison of the Verigene Clostridium difficile, Simplexa C. difficile Universal Direct, BD MAX Cdiff, and Xpert C. difficile assays for the detection of toxigenic C. difficile." Diagnostic Microbiology and Infectious Disease 80, no. 1 (September 2014): 13–18. http://dx.doi.org/10.1016/j.diagmicrobio.2014.06.001.

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Cannon, Cara M., Jackson S. Musuuza, Anna K. Barker, Megan Duster, Mark B. Juckett, Aurora E. Pop-Vicas, and Nasia Safdar. "Risk of Clostridium difficile Infection in Hematology-Oncology Patients Colonized With Toxigenic C. difficile." Infection Control & Hospital Epidemiology 38, no. 06 (April 11, 2017): 718–20. http://dx.doi.org/10.1017/ice.2017.48.

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The prevalence of colonization with toxigenic Clostridium difficile among patients with hematological malignancies and/or bone marrow transplant at admission to a 566-bed academic medical care center was 9.3%, and 13.3% of colonized patients developed symptomatic disease during hospitalization. This population may benefit from targeted C. difficile infection control interventions. Infect Control Hosp Epidemiol 2017;38:718–720
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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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Hussain, Zeiad I., Neil Todd, Simon Adams, and Stevan G. Stojkovic. "Prevalence of Clostridium Difficile in Excluded Colons." American Surgeon 78, no. 4 (April 2012): 408–13. http://dx.doi.org/10.1177/000313481207800429.

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Clostridium difficile infection is associated with substantial morbidity and mortality, increased duration of hospitalization, and a marked economic impact. Several case reports and case series have described C. difficile infection in excluded bowels or immediately after reversal of defunctioning ileostomy. The aim of this prospective study is to detect whether the excluded colon is associated with a higher rate of C. difficile colonization than the normal population, which may increase the risk of C. difficile infection. Patients with defunctioning loop ileostomy, undergoing closure of ileostomy to restore bowel continuity, were prospectively recruited. Two stool samples were collected from the ileostomy effluent before closure of ileostomy and two after the procedure including the first bowel movement. All samples were cultured for C. difficile and analyzed for toxins A and B by a Premier EIA test. Demographic data and possible confounding factors were observed and recorded. Twenty-fine adult patients were recruited to this study; five patients were subsequently excluded. Two patients had positive stool cultures for C. difficile in the postoperative samples and another patient developed clinical pseudomembranous colitis with positive toxin. This indicates a possible colonization rate of 3 to 38 per cent (95% confidence interval). Four observed cases out of the 20 subjects taking part in this study would confidently conclude that C. difficile colonization in the excluded colon is 6 to 44 per cent, i.e., higher than the incidence in the healthy adult population, which is 3 per cent. However, the findings of this study prompt larger and well-powered studies to confirm these findings.
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Kelly, C. P., C. Pothoulakis, F. Vavva, I. Castagliuolo, E. F. Bostwick, J. C. O'Keane, S. Keates, and J. T. LaMont. "Anti-Clostridium difficile bovine immunoglobulin concentrate inhibits cytotoxicity and enterotoxicity of C. difficile toxins." Antimicrobial Agents and Chemotherapy 40, no. 2 (February 1996): 373–79. http://dx.doi.org/10.1128/aac.40.2.373.

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Clostridium difficile diarrhea and colitis result from the actions of bacterial exotoxins on the colonic mucosa. This study examined the ability of hyperimmune bovine colostral antibodies to neutralize the biological effects of these toxins. Anti-C. difficile bovine immunoglobulin concentrate was prepared from the colostral milk of Holstein cows previously immunized with C. difficile toxoids. The anti-C. difficile bovine immunoglobulin concentrate contained high levels of bovine immunoglobulin G specific for C. difficile toxins A and B, as evaluated by enzyme-linked immunosorbent assay. Anti-C. difficile bovine immunoglobulin concentrate neutralized the cytotoxic effects of purified toxin A and toxin B on cultured human fibroblasts, whereas control bovine immunoglobulin concentrate had little toxin-neutralizing activity. Anti-C. difficile bovine immunoglobulin concentrate also blocked the binding of toxin A to its enterocyte receptor and inhibited the enterotoxic effects of C. difficile toxins on the rat ileum, as measured by an increased rat ileal loop weight/length ratio (63% inhibition; P < 0.01), increased mannitol permeability (92% inhibition; P < 0.01), and histologic grading of enteritis (P < 0.01 versus nonimmune bovine immunoglobulin concentrate). Thus, anti-C. difficile bovine immunoglobulin concentrate neutralizes the cytotoxic effects of C. difficile toxins in vitro and inhibits their enterotoxic effects in vivo. This agent may be clinically useful in the prevention and treatment of C. difficile diarrhea and colitis.
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Dormann, Arno, and Thomas Weinke. "Clostridium-difficile-Infektionen – Ein zunehmendes Problem in deutschen Krankenhäusern." Der Klinikarzt 44, S 01 (January 2015): 2–10. http://dx.doi.org/10.1055/s-0035-1544991.

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ZusammenfassungDie Inzidenz durch Clostridium difficile ausgelöster Enterokolitiden (C.-difficile-Infektionen, CDI) hat in den letzten Jahren in deutschen Krankenhäusern deutlich zugenommen. Abhängig von verschiedenen Risikofaktoren kann die Infektion sehr schwer oder sogar lebensbedrohlich verlaufen. Tritt also eine nosokomiale Diarrhö auf, sollte daher immer an eine Infektion mit Clostridium difficile gedacht und die Diagnostik und gegebenenfalls eine angemessene Therapie zeitnah eingeleitet werden. Eine besondere Herausforderung sind die mit einer C.-difficile-Infektion einhergehenden hohen Rückfallraten. Dabei unterscheiden sich die bei schweren Verläufen oder erhöhtem Rückfallrisiko empfohlenen Antibiotika Vancomycin und Fidaxomicin hinsichtlich der Wahrscheinlichkeit eines Rückfalls. Einer der Hauptrisikofaktoren für eine CDI ist der Einsatz von Breitspektrumantibiotika, weshalb ihr sorgsamer und differenzierter Einsatz empfohlen wird, um Clostridium-difficile-Infektionen möglichst einzudämmen. Hygienemaßnahmen wie das gründliche Waschen der Hände mit Wasser und Seife tragen dazu bei, die Verbreitung der C.-difficile-Sporen zu verhindern.
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38

Mahida, Y. R. "New concepts in C. difficile management." British Medical Bulletin 131, no. 1 (September 2019): 109–18. http://dx.doi.org/10.1093/bmb/ldz029.

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Abstract Background Clostridium difficile infection is transmitted via spores, and the disease is mediated via secreted toxins. It represents a significant healthcare problem, and clinical presentation can range from asymptomatic carriage to life-threatening pseudomembranous colitis. Sources of data publications in the field, with a focus on recent developments and concepts. Areas of agreement infection control measures, antibiotic stewardship and current management of the initial episode of C. difficile infection. Areas of controversy selection and sequence of interventions for the management of recurrent C. difficile infection; management of persistent carriers of toxigenic C. difficile in patients at high risk of subsequent C. difficile infection. Growing points use of faecal microbiota transplantation for recurrent C. difficile infection. Areas timely for developing research role of specific microbiota-mediated interventions and vaccination in the treatment and prevention of C. difficile infection.
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Salcedo, J., S. Keates, C. Pothoulakis, M. Warny, I. Castagliuolo, J. T. LaMont, and C. P. Kelly. "Intravenous immunoglobulin therapy for severe Clostridium difficile colitis." Gut 41, no. 3 (September 1, 1997): 366–70. http://dx.doi.org/10.1136/gut.41.3.366.

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Background—Many individuals have serum antibodies against Clostridium difficile toxins. Those with an impaired antitoxin response may be susceptible to recurrent, prolonged, or severe C difficile diarrhoea and colitis.Aims—To examine whether treatment with intravenous immunoglobulin might be effective in patients with severe pseudomembranous colitis unresponsive to standard antimicrobial therapy.Patients—Two patients with pseudomembranous colitis not responding to metronidazole and vancomycin were given normal pooled human immunoglobulin intravenously (200–300 mg/kg).Methods—Antibodies against C difficile toxins were measured in nine immunoglobulin preparations by ELISA and by cytotoxin neutralisation assay.Results—Both patients responded quickly as shown by resolution of diarrhoea, abdominal tenderness, and distension. All immunoglobulin preparations tested contained IgG against C difficile toxins A and B by ELISA and neutralised the cytotoxic activity of C difficile toxins in vitro at IgG concentrations of 0.4–1.6 mg/ml.Conclusion—Passive immunotherapy with intravenous immunoglobulin may be a useful addition to antibiotic therapy for severe, refractory C difficile colitis. IgG antitoxin is present in standard immunoglobulin preparations andC difficile toxin neutralising activity is evident at IgG concentrations which are readily achieved in the serum by intravenous immunoglobulin administration.
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Alvarez-Perez, S., P. Alba, J. L. Blanco, and M. E. Garcia. "Detection of toxigenic Clostridium difficile in pig feces by PCR." Veterinární Medicína 54, No. 8 (September 22, 2009): 360–66. http://dx.doi.org/10.17221/76/2009-vetmed.

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: <I>Clostridium difficile</I> is considered an important uncontrolled cause of neonatal diarrhea. Also, the presence of bacteria in the feces of the animal could represent a zoonosic risk for the contamination of meat products. Therefore, it is necessary to have procedures available for the early detection of <I>C. difficile</I> in animals. The current study describes a new semi-automated procedure for the recovery of <I>C. difficile</I> DNA from pig feces and subsequent amplification by polymerase chain reaction (PCR) of three different sequences: the triose phosphate isomerase gene <I>tpi</I>, specific for this bacterial species, and the <I>tcdA</I> and <I>tcdB</I> genes, which code for the A and B toxins of <I>C. difficile</I>, respectively. Twenty-two fecal samples microbiologically positive for <I>C. difficile</I> were used. The <I>tpi</I> and <I>tcdA</I> genes were amplified in all of them. The internal fragment of <I>tcdB</I> was detected from 21 of these extracts; the negative sample gave a positive result when a different primer pair was used. None of the 10 DNA extracts obtained from culture-negative samples gave a positive result. The method presented in this article eliminates the interference caused by the possible presence of PCR inhibitors. To the authors’ knowledge, this is the first description of a PCR procedure for detection of <I>C. difficile</I> DNA from domestic animal feces.
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Etienne-Mesmin, Lucie, Benoit Chassaing, Oluwaseyi Adekunle, Lisa M. Mattei, Frederic D. Bushman, and Andrew T. Gewirtz. "Toxin-positive Clostridium difficile latently infect mouse colonies and protect against highly pathogenic C. difficile." Gut 67, no. 5 (February 20, 2017): 860–71. http://dx.doi.org/10.1136/gutjnl-2016-313510.

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ObjectiveClostridium difficile is a toxin-producing bacterium and a leading cause of antibiotic-associated disease. The ability of C. difficile to form spores and infect antibiotic-treated persons at low multiplicity of infection (MOI) underlies its large disease burden. However, C. difficile-induced disease might also result from long-harboured C. difficile that blooms in individuals administered antibiotics.DesignMice purchased from multiple vendors and repeatedly testing negative for this pathogen by quantitative PCR bloomed C. difficile following antibiotic treatment. This endogenous C. difficile strain, herein termed LEM1, which formed spores and produced toxin, was compared with highly pathogenic C. difficile strain VPI10463.ResultsWhole-genome sequencing revealed that LEM1 and VPI10463 shared 95% of their genes, including all known virulence genes. In contrast to VPI10463, LEM1 did not induce overt disease when administered to antibiotic-treated or germ-free mice, even at high doses. Rather, blooms of LEM1 correlated with survival following VPI10463 inoculation, and exogenous administration of LEM1 before or shortly following VPI10463 inoculation prevented C. difficile-induced death. Accordingly, despite similar growth properties in vitro, LEM1 strongly outcompeted VPI10463 in mice even at 100-fold lower inocula.ConclusionsThese results highlight the difficulty of determining whether individual cases of C. difficile infection resulted from a bloom of endogenous C. difficile or a new exposure to this pathogen. In addition to impacting the design of studies using mouse models of C. difficile-induced disease, this study identified, isolated and characterised an endogenous murine spore-forming C. difficile strain able to decrease colonisation, associated disease and death induced by a pathogenic C. difficile strain.
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42

Gil, Gaby S., Shobhana Chaudhari, Ahmed Shady, Ana Caballes, and Joe Hong. "Blastocystissp. Infection Mimicking Clostridium Difficile Colitis." Case Reports in Infectious Diseases 2016 (2016): 1–2. http://dx.doi.org/10.1155/2016/7264387.

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We report an unusual case of severe diarrhea related toBlastocystissp. infection in a patient with end stage renal disease on hemodialysis. The patient was admitted due to profuse diarrhea associated with fever and leukocytosis. Pertinent stool work-up such as leukocytes in stool, stool culture, clostridium difficile toxin B PCR, and serology for hepatitis A, hepatitis B, and hepatitis C and cytomegalovirus screening were all negative. Ova and parasite stool examination revealedBlastocystissp. The patient was given intravenous metronidazole with clinical improvement by day three and total resolution of symptoms by day ten.
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Chai, Changhoon, Kyung-Soo Lee, Goo-Sang Imm, Young Soon Kim, and Se-Wook Oh. "Inactivation of Clostridium difficile spore outgrowth by synergistic effects of nisin and lysozyme." Canadian Journal of Microbiology 63, no. 7 (July 2017): 638–43. http://dx.doi.org/10.1139/cjm-2016-0550.

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Inactivating Clostridium difficile spores is difficult, as they are resistant to heat, chemicals, and antimicrobials. However, this note describes inactivation of C. difficile spore outgrowth by incubation in a solution containing a germinant (1% (m/v) sodium taurocholate), co-germinants (1% (m/v) tryptose and 1% (m/v) NaCl), and natural antimicrobials (20 nmol·L–1 nisin and 0.2 mmol·L–1 lysozyme). Clostridium difficile spores were resistant to nisin and lysozyme but became susceptible during germination and outgrowth triggered and promoted by sodium taurocholate, tryptose, and NaCl. The degree of inactivation of germinated and outgrowing C. difficile spores by both nisin and lysozyme was greater than the sum of that by nisin and lysozyme individually, suggesting synergistic inactivation of C. difficile spores. The germinant, co-germinants, and natural antimicrobials used in this study are safe for human contact and consumption. Therefore, these findings will facilitate the development of a safe and effective method to inactivate C. difficile spore.
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Zhang, Wen, Ying Cheng, Pengcheng Du, Yuanyuan Zhang, Hongbing Jia, Xianping Li, Jing Wang, et al. "Genomic study of the Type IVC secretion system in Clostridium difficile: understanding C. difficile evolution via horizontal gene transfer." Genome 60, no. 1 (January 2017): 8–16. http://dx.doi.org/10.1139/gen-2016-0053.

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Clostridium difficile, the etiological agent of Clostridium difficile infection (CDI), is a gram-positive, spore-forming bacillus that is responsible for ∼20% of antibiotic-related cases of diarrhea and nearly all cases of pseudomembranous colitis. Previous data have shown that a substantial proportion (11%) of the C. difficile genome consists of mobile genetic elements, including seven conjugative transposons. However, the mechanism underlying the formation of a mosaic genome in C. difficile is unknown. The type-IV secretion system (T4SS) is the only secretion system known to transfer DNA segments among bacteria. We searched genome databases to identify a candidate T4SS in C. difficile that could transfer DNA among different C. difficile strains. All T4SS gene clusters in C. difficile are located within genomic islands (GIs), which have variable lengths and structures and are all conjugative transposons. During the horizontal-transfer process of T4SS GIs within the C. difficile population, the excision sites were altered, resulting in different short-tandem repeat sequences among the T4SS GIs, as well as different chromosomal insertion sites and additional regions in the GIs.
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Moreira, Bárbara de Oliveira, Luana Silva Pais, and Lívia de Almeida Costa. "Diarreia causada por Clostridium difficile: recentes avanços." HU Revista 43, no. 2 (July 24, 2018): 155–61. http://dx.doi.org/10.34019/1982-8047.2017.v43.2653.

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A infecção causada por Clostridium difficile (C. difficile), um dos agentes causadores de diarréia aguda e recorrente, tem como principal fator de risco o uso de antimicrobianos. Recentemente, houve um aumento da incidência e da mortalidade desta afecção. Clinicamente, a mesma pode manifestar-se desde um quadro de diarreia aquosa leve até a forma grave de colite pseudomembranosa. O objetivo deste artigo é apontar as mudanças epidemiológicas da infecção pelo C. difficile, além de rever fatores de risco, manifestações clínicas, métodos diagnósticos, tratamento e prevenção desta infecção. O aumento na gravidade da infecção causada pelo C. difficile é relacionado a uma nova cepa hipervirulenta, BI/NAPI/Ribotipo 027, que apresenta maior capacidade de produção de toxinas. Essa nova cepa, mais virulenta, ainda não foi detectada no Brasil, porém como já foi identificada em outros países da América, alerta para a preocupante capacidade de disseminação universal. Essa revisão é baseada em artigos publicados nos últimos 10 anos, utilizando como base de dados o PubMed e o Scielo (Scientific Eletronic Library Online), com as palavras-chave: Epidemiologia, diarreia, Clostridium difficile e cepa hipervirulenta.
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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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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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48

Kocic, Branislava, and Predrag Stojanovic. "Clinical importance of Clostridium difficile finding in hospitalized patients." Medical review 61, no. 11-12 (2008): 632–37. http://dx.doi.org/10.2298/mpns0812632k.

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Introduction Clostridium difficile infections predominatelly occur among hospitalized patients. The aim of this study was to evaluate the importance of finding the isolate of Clostridium difficile cultured from the stool of hospitalized patients. Material and methods Material consisted of 100 patients with at least one liquid stool samples and control group with form stool. Every patient spent minimum 48h in hospital before the sampling. The material was immediately cultured on mediums for isolation of enteric pathogens, and on selective CCFA medium (Biomedics) for Clostridium difficile in anaerobic condition. Diagnosis of Clostridium difficile toxin in stool samples was achieved by ELISA-RIDASCREEN Clostridium difficile Toxin A/B test (R-Biopharm). Results One-hundred forty one stool samples of patients in Clinical Center Nis were cultivated and examined for C. difficile. The bacteria was isolated in seven patients from the clinical group. In four (57.14%) patients, the presence of C. difficile toxin in stool was established. The bacteria was diagnosed from the stool samples of five patients from the control group, but the toxin was not found in their stool samples. Discussion The results performed at the Institute for Public Health Nis are in accordance with previously published results that all patients with positive findings of Clostridium difficile toxin in stool samples were on antibiotic treatment longer than 14 days. By analyzing the patient's stay in hospital and duration of antibiotic treatment, we observed the statistically significant difference in findings between the patients with CDAD and the patients from the control group with positive bacteria. Conclusion The study confirms the importance of finding Clostridium difficile associated disease in four (4%) hospitalized patients.
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Seugendo, Mwanaisha, Aldofine Hokororo, Rogatus Kabyemera, Delfina R. Msanga, Mariam M. Mirambo, Vitus Silago, Uwe Groß, and Stephen E. Mshana. "High Clostridium difficile Infection among HIV-Infected Children with Diarrhea in a Tertiary Hospital in Mwanza, Tanzania." International Journal of Pediatrics 2020 (August 28, 2020): 1–7. http://dx.doi.org/10.1155/2020/3264923.

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Clostridium difficile causes a million of illnesses each year worldwide and can affect people of all ages. Limited data exist on the prevalence of C. difficile infections (CDI) among children below five years of age in developing countries. This study is aimed at determining the prevalence, associated factors, and outcome of the Clostridium difficile infection among children with diarrhea attending a tertiary hospital in Mwanza, Tanzania. Stool samples were collected and cultured anaerobically to isolate Clostridium difficile, followed by C. difficile toxin A and B assay and ribotyping. A total of 301 children with diarrhea were enrolled. A total of 22 (7.31%, 95% CI: 0.89-0.95) nonrepetitive stool samples were positive for Clostridium difficile. Eighteen (81%) of C. difficile isolates were toxigenic, and 16 (72.7%) had unknown ribotypes. Independent predictors of positive C. difficile were as follows: positive HIV status, hospital stay of more than four days, high stool leukocyte count, and watery stool. Clostridium difficile-positive children had significantly higher median duration of the diarrhea than those without C. difficile. Clinicians should consider C. difficile as a possible cause of diarrhea in children living in developing countries and institute appropriate management to prevent associated morbidities and mortalities. Furthermore, there is a need of joint effort to improve C. difficile diagnosis and surveillance in developing countries to establish the unknown epidemiology of CDI in these countries.
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Han, Sang Bong, Jiyoung Chang, Sang Hyun Shin, Kang Gyun Park, Gun Dong Lee, Yong Gyu Park, and Yeon-Joon Park. "Performance of chromID Clostridium difficile Agar Compared with BBL C. difficile Selective Agar for Detection of C. difficile in Stool Specimens." Annals of Laboratory Medicine 34, no. 5 (September 1, 2014): 376–79. http://dx.doi.org/10.3343/alm.2014.34.5.376.

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