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PubMed2001

Isolation of Clostridium innocuum from cases of recurrent diarrhea in patients with prior Clostridium difficile associated diarrhea.

Clostridium innocuum isolates resistant to vancomycin (MIC values of 16-24 microg/mL) were isolated from three patients with recurrent Clostridium difficile -associated diarrhea (CDAD). We discuss the clinical significance and problems associated with the identification and differentiation of these two clostridial species, which may result in misdiagnosis of patients.

Clostridioides difficile↗
PubMed2003

Gastrointestinal disorders and the critically ill. Clostridium difficile infection and pseudomembranous colitis.

Clostridium difficile causes a spectrum of diseases ranging from diarrhoea to pseudomembranous colitis, primarily in the hospitalized elderly, although community-acquired infection is probably under-documented. Host factors are increasingly recognized as critical determinants of disease expression. Exposure to antibiotics, particularly those adversely affecting anaerobic gut flora, appears to create a niche which is exploited by C. difficile. Several retrospective and intervention studies have indicated that third-generation cephalosporins have a high propensity to induce C. difficile diarrhoea. Conversely, some broad-spectrum antibiotics, including ureidopenicillins (e.g. piperacillin-tazobactam) and ciprofloxacin, are less likely to induce C. difficile infection. Effective control of C. difficile in the hospital requires both antibiotic control and prevention of environmental seeding and bacterial spread. Epidemic C. difficile strains are widely distributed in the hospital environment, both as a cause and result of nosocomial diarrhoea. Current treatment options are antibiotic-based, which is less than ideal. Although many biotherapeutic approaches have been tried few have shown real benefit.

Clostridioides difficile↗
PubMed1992

High prevalence of Clostridium difficile diarrhoea during intensive chemotherapy for disseminated germ cell cancer.

A prospective, consecutive study of the aetiology of treatment-associated diarrhoea was conducted in 25 patients with disseminated germ cell cancer treated with intensive chemotherapy. Clostridium difficile was isolated in 45% of the diarrhoea episodes, which makes this species the most important bacterial pathogen in the development of clinically significant diarrhoea in this group of immunocompromised patients.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1993

The microecology of Clostridium difficile.

An understanding of the microecology of Clostridium difficile provides for a better understanding of the disease that this organism causes. C. difficile is not a significant component of the microflora in the colon of healthy adult humans or animals; however, it can establish large populations in antibiotic-treated or gnotobiotic animals and in infants before they acquire a complete flora. Major factors that determine whether or not disease develops are: (1) the size of the C. difficile populations; (2) the toxigenicity of the colonizing strain; (3) the presence of other organisms that affect toxin expression or activity; (4) susceptibility of the host; and possibly (5) a strain's adhesion to colonic epithelium. The rest of the colonic flora determines the size of the C. difficile population, at least in part by limiting available nutrients. In outbreaks, most C. difficile disease is caused by nosocomial strains. Environmental contamination with spores and spread via the hands of health care workers have been implicated in transmission. Information with regard to this organism's microecology suggests alternative approaches to the control of disease.

Animals↗
PubMed2004

Coinfection with Giardia lamblia and Clostridium difficile after use of ranitidine.

A 49-year-old man presented with a 3-week history of vomiting and diarrhea. He reported foamy stools but no blood or melena and had crampy epigastric pain. He denied usage of antibiotics. He had been taking ranitidine for intermittent epigastric pain for the last few months and noted an 11-pound weight loss during the 3 weeks before admission. Stool was positive for Clostridium difficile toxin and Giardia lamblia antigen. Cultures and occult blood tests were negative. Oral metronidazole, 500 mg 3 times a day, was administered, and the patient was hydrated. The diarrhea resolved, and patient was discharged on the fourth hospital day. Prior antibiotic therapy is the most common risk factor for C difficile colitis. This patient developed concomitant infection with C difficile and G lamblia while he used ranitidine. He had no other risk factors for these infections. Hence, we propose that ranitidine-induced hypochlorhydria predisposed this patient to the enteric infections.

Achlorhydria↗
PubMed2005

Revised nomenclature of Clostridium difficile toxins and associated genes.

Several different nomenclatures have been applied to the Clostridium difficile toxins and their associated genes. This paper summarizes the new nomenclature that has been agreed to by the research groups currently active in the field. The revised nomenclature includes C. difficile toxins and other related large clostridial toxins produced by Clostridium sordellii and Clostridium novyi, and corresponding toxin genes, as well as toxin production types of C. difficile strains.

Bacterial Proteins↗
PubMed2002

Differential expression and polarized secretion of CXC and CC chemokines by human intestinal epithelial cancer cell lines in response to Clostridium difficile toxin A.

Intestinal epithelial cells are the initial sites of host response to Clostridium difficile infection and can play a role in signaling the influx of inflammatory cells. To further explore this role, the regulated expression and polarized secretion of CXC and CC chemokines by human intestinal epithelial cells were investigated. An expression of the CXC chemokines, including IL-8 and growth-related oncogene (GRO)-alpha, and the CC chemokine monocyte chemoattractant protein (MCP)-1 from HT-29 cells increased in the 1-6 hr following C. difficile toxin A stimulation, assessed by quantitative RT-PCR. In contrast, the expression of neutrophil activating protein-78 (ENA-78) was delayed for 18 hr. The up-regulated mRNA expression of chemokines was paralleled by the increase of protein levels. However, the expression of macrophage inflammatory protein (MIP)-1alpha, RANTES (regulated on activation normal T cells expressed and secreted), and interferon-gamma-inducible protein-10 (IP-10) was not changed in HT-29 or Caco-2 cells stimulated with toxin A. Upon stimulation of the polarized Caco-2 epithelial cells in a transwell chamber with toxin A, CXC and CC chemokines were released predominantly into the basolateral compartment. Moreover, the addition of IFN-gamma and TNF-alpha to toxin A stimulated Caco-2 cells increased the basolateral release of CC chemokine MCP-1. In contrast, IFN-gamma and TNF-alpha had no effect on the expression of the CXC chemokines IL-8 and GRO-alpha. These results suggest that a CXC and CC chemokine expression from epithelial cells infected with C. difficile may be an important factor in the mucosal inflammatory response.

Bacterial Toxins↗
PubMed1999

Saccharomyces boulardii protease inhibits the effects of Clostridium difficile toxins A and B in human colonic mucosa.

Saccharomyces boulardii is a nonpathogenic yeast used in the treatment of Clostridium difficile diarrhea and colitis. We have reported that S. boulardii inhibits C. difficile toxin A enteritis in rats by releasing a 54-kDa protease which digests the toxin A molecule and its brush border membrane (BBM) receptor (I. Castagliuolo, J. T. LaMont, S. T. Nikulasson, and C. Pothoulakis, Infect. Immun. 64:5225-5232, 1996). The aim of this study was to further evaluate the role of S. boulardii protease in preventing C. difficile toxin A enteritis in rat ileum and determine whether it protects human colonic mucosa from C. difficile toxins. A polyclonal rabbit antiserum raised against purified S. boulardii serine protease inhibited by 73% the proteolytic activity present in S. boulardii conditioned medium in vitro. The anti-protease immunoglobulin G (IgG) prevented the action of S. boulardii on toxin A-induced intestinal secretion and mucosal permeability to [3H]mannitol in rat ileal loops, while control rabbit IgG had no effect. The anti-protease IgG also prevented the effects of S. boulardii protease on digestion of toxins A and B and on binding of [3H]toxin A and [3H]toxin B to purified human colonic BBM. Purified S. boulardii protease reversed toxin A- and toxin B-induced inhibition of protein synthesis in human colonic (HT-29) cells. Furthermore, toxin A- and B-induced drops in transepithelial resistance in human colonic mucosa mounted in Ussing chambers were reversed by 60 and 68%, respectively, by preexposing the toxins to S. boulardii protease. We conclude that the protective effects of S. boulardii on C. difficile-induced inflammatory diarrhea in humans are due, at least in part, to proteolytic digestion of toxin A and B molecules by a secreted protease.

Animals↗
PubMed2006

Epithelial cell I kappa B-kinase beta has an important protective role in Clostridium difficile toxin A-induced mucosal injury.

Toxin A released by Clostridium difficile interacts with the single layer of intestinal epithelial cells that lines the host's intestinal tract and leads to mucosal damage and inflammation that manifests clinically as antibiotic-associated diarrhea and pseudomembranous colitis. Activation of the transcription factor NF-kappaB in intestinal epithelial cells is important for regulating the expression of epithelial cell proinflammatory genes and cell survival. However, the role of NF-kappaB activation in the pathogenesis of C. difficile toxin A-induced colitis is unknown. To determine the functional importance in vivo of NF-kappaB activation in intestinal epithelium in the pathogenesis of C. difficile-induced colitis, we used mutant mice that do not activate the classical NF-kappaB signaling pathway in intestinal epithelial cells due to a conditional deficiency in those cells of the IkappaB-kinase beta (IKKbeta) subunit of IKK. C. difficile toxin A challenge of intestinal loops in intestinal epithelial cell IKKbeta-deficient mice induced a rapid and significant increase in intestinal epithelial apoptosis compared with littermate controls. This was accompanied by a significant increase in acute mucosal inflammation, mucosal injury, luminal fluid secretion, and bacterial translocation. We conclude that activation of intestinal epithelial cell NF-kappaB by toxin A plays an important host mucosal protective role after C. difficile toxin A exposure that is mediated, at least in part, through promoting epithelial cell survival by abrogating epithelial cell apoptosis.

Animals↗
PubMed1999

[Isolation of toxigenic strains of Clostridium difficile and enterotoxin producing Bacteroides fragilis from fecal specimens of patients suspected of antibiotic associated diarrhoea].

Fifty faecal samples from patients suspected of AAD (antibiotic associated diarrhoea) were studied for Clostridium difficile and enterotoxin producing Bacteroides fragilis (ETBF). Using TCD (Becton-Dickinson) and C. difficile Toxin A test (Oxoid) in 34% of specimens the presence of toxin A was detected. From all specimens 25 C. difficile strains were isolated. All isolated strains produced toxin B in vitro which was shown in Mc Coy cytotoxicity test. Eighteen strains only were toxin A positive in vitro. From all isolated C. difficile strains 28% were tox A (-) tox B (+). By means of PCR presence of toxin A and toxin B genes was tested directly in faecal samples and in strains. From the same 50 faecal samples 17 B. fragilis strains were isolated. Four of them produced the enterotoxin (fragilisin) which was detected on the HT 29/C1 cell line. Genes of fragilisin were found in strains and directly in faecal samples. Toxin producing C. difficile and B. fragilis (ETBF) together were found in 3 samples. From one faecal sample only ETBF was cultured.

Adult↗
PubMed2001

[Clostridium difficile bacteremia].

BACKGROUND: Extra-digestive manifestations of Clostridium difficile infection are very uncommon. Exceptional cases of C. difficile bacteremia or severe sepsis have been described in intensive care patients, demonstrating the capacity of this agent to generate generalized infection. CASE REPORT: C. difficile bacteremia occurred in a 66-year-old immunodepressed patient treated for acute myeloblastic leukemia. Bacteremia was associated with a abscess of the anal margin. Outcome was favorable after treatment with metronidosole. DISCUSSION: Clostridium difficile is generally selected by prior antibiotic treatment. It is the principal agent of nosocomial diarrhea. In immunodepressed patients, systemic dissemination is a rare but possible development.

Aged↗
PubMed1992

[Eremomycin in the treatment of antibiotic-associated colitis in golden hamsters].

The efficacy of eremomycin, a new glycopeptide antibiotic, was studied on a model of antibiotic-associated colitis in golden hamsters. The colitis was induced by intraperitoneal or intragastric administration of lincomycin. In a dose of 100 mg/kg administered orally once a day for 5 days eremomycin protected the animals from the lincomycin-induced colitis: some animals survived, the others died in later periods. When the animals were infected with a pathogenetic strain of Clostridium difficile followed by exposure to lincomycin the use of eremomycin produced the similar effect.

Administration, Oral↗
PubMed1991

Clostridium difficile and its cytotoxin in hospitalized children with acute diarrhea.

A total of 498 children, aged 0-14 years, admitted at the B.C. Roy Memorial Hospital for Children, Calcutta, were investigated for the occurrence of Clostridium difficile and its cytotoxin. Of the children in the investigation, 369 suffered from acute diarrhea. Only 8.4% of these children had C. difficile in fecal samples and in vitro cytotoxin was demonstrated in 7%. In 27 (7.3%) of the patients with acute diarrhea C. difficile was isolated as the only pathogen. In contrast, among 129 control children not suffering from acute diarrhea, only 4 (3.1%) harboured C. difficile. Isolation of C. difficile was significantly higher in children under one year of age. None of these patients had any history of prior antibiotic therapy.

Acute Disease↗
PubMed1995

Diarrhea in the intensive care patient.

Approximately one third of patients admitted to the ICU develop diarrhea during their hospitalization. Diarrhea can lead to further complications, such as volume depletion and wound infection, and can significantly increase medical costs. The most common causative factors are medications, enteral feedings, and C. difficile infections. These may be implicated alone or in combination. Further investigations of the pathophysiology of ICU diarrhea as well as potential therapies are needed to clarify the proper approach to this important and complex problem.

Clostridioides difficile↗
PubMed1997

Five spontaneous deaths associated with Clostridium difficile in a colony of cotton-top tamarins (Saguinus oedipus).

Clostridium difficile toxin was detected in the feces of five cotton-top tamarins (Saguinus oedipus) that died spontaneously over a period of 10 weeks. Deaths occurred subsequent to antibiotic therapy for infectious diarrhea associated with Campylobacter spp. Relevant clinical signs of disease prior to death included weight loss, watery diarrhea, hematochezia, weakness, and sudden collapse. On histologic examination of the colon at necropsy, pseudomembranous colitis was evident in two cases, a lesion consistent with C. difficile lesions in humans. This finding prompted submission of feces for C. difficile toxin analysis from these five cases. Four of the tamarins were from a single room, and the fifth was housed nearby. The proximity of the cases raises the possibility of environmental contamination by resistant C. difficile spores or fecal spread of the organism as reported in hospitals, day-care centers, and nurseries. The relative importance of C. difficile and its potential role as an unrecognized cause of enteric disease secondary to antibiotic therapy in nonhuman primates is discussed.

Animals↗
PubMed1998

[Outbreak of nosocomial diarrhea by Clostridium difficile in a department of internal medicine].

BACKGROUND: Clostridium difficile (DCD) is the main etiologic agent of nosocomial diarrhea of infectious origin. Most of the cases of DCD have been detected in a hospital environment. PATIENTS, MATERIAL AND METHODS: From October to November 1996 five cases of nosocomial diarrhea were detected with the presence of the toxin A of Clostridium difficile being observed in the stools. These patients were compared with a group of 19 patients without diarrhea (controls) who were admitted to the same ward during the same period as the patients with DCD. RESULTS: The hospital stay of the cases was greater (25 +/- 8 days) than that of the controls (14 +/- 10 days; p < 0.05). One hundred percent of the cases received antibiotics during admission (2 +/- 1.2 antibiotics per patient), versus 68% of the controls (1.1 +/- 0.9 antibiotics per patient, p > 0.05). The length of antibiotic treatment prior to the onset of the symptoms was 8 +/- 3 days (range 7-11 days). The type of antibiotic administered was similar in both groups. More of the cases with DCD (60%) had vesicle catheterization than the controls (11%, p < 0.05). All the patients with DCD presented abdominal pain and several liquid stools per day without blood or pus (3.2 +/- 0.45 stools per patient) and 2 (40%) fever. The mean length of diarrhea was 5.6 +/- 3.6 days. The serum albumin concentration on the first day of admission was significantly lower in the cases of DCD (2.9 +/- 0.4 mg/dl) than in the controls (3.3 +/- 3.4 mg/dl, p < 0.05). All the cases received antibiotic treatment for Clostridium difficile (oral metronidazol or vancomycin) with good clinical evolution. CONCLUSIONS: The patients with DCD had more often had vesicle catherization and presented a lower serum albumin concentration than the controls.

Adult↗
PubMedDate not supplied

Risk factors for the development of Clostridium difficile toxin-associated diarrhoea: a pilot study.

This study was a pilot investigation of risk factors for the development of Clostridium difficile toxin-associated diarrhoea and in particular the differential influence of antimicrobial agents. The study was a retrospective case-control design conducted at Freeman Hospital, Newcastle upon Tyne. Cases were inpatients with stool positive C. difficile toxin diarrhoea and two controls were drawn for each case matched for age (+/- 5 years) and type of admission (emergency or elective). Using conditional logistic regression analysis, cephalosporins and erythromycin were found to be statistically significantly associated with Clostridium difficile toxin associated-diarrhoea. The results form the basis for designing a larger, prospective study.

Adult↗
PubMed1997

Intracellular transport and processing of protein toxins produced by enteric bacteria.

Bacterial toxins are associated with disease in humans and animals. Toxins can either be preformed in food or produced by bacteria in the intestine. There are two types of toxins: heat-labile protein toxins and heat stabile toxins. Heat labile toxins are produced by Bacillus cereus, Clostridium perfringens, Escherichia coli, and Vibrio cholerae, and heat-stabile enterotoxins consisting of relatively few amino acids are produced by Escherichia coli and acts by activation of guanylate cyclase. Similarly, heat-stabile entero-toxins are also produced by Staphylococcus aureus, a common cause of food poisoning in the United States, and Yersenia enterocolitica. Protein toxins produced by enteric bacteria can intoxicate intestinal cells and can also be taken up from the gut and reach other cells in the body. For example the Shiga-like toxins (vero-toxins) can intoxicate endothelial cells in the kidney and cause kidney failure. Intracellular transport and processing of a few of the protein toxins produced by enteric bacteria, namely Clostridium difficile toxin A and B, cholera toxin and the related heat-labile toxin produced by Escherichia coli, and Shiga toxin and Shiga-like toxins are presented.

Animals↗