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PubMed1992

Molecular, immunological, and biological characterization of a toxin A-negative, toxin B-positive strain of Clostridium difficile.

A cytotoxigenic Clostridium difficile strain that fails to produce toxin A but causes hemorrhage and bloody fluid accumulation in ligated ileal loops of rabbits and hemorrhage and diarrhea in hamsters is described. The lack of reaction of DNA from this strain in hybridization studies with a toxin A gene-specific 4.5-kb probe and polymerase chain reaction studies with six toxin A-specific primers indicate the absence of the toxin A gene. The cytotoxin produced by this strain was not responsible for the enterotoxic or hemorrhagic activity and shared characteristics with toxin B, i.e., its cytotoxicity was neutralized by antibodies to toxigenic strains of C. difficile and Clostridium sordellii. Polymerase chain reaction studies with toxin B-specific primers showed that the DNA from this strain produced a 690-bp product in addition to the expected 591-bp product.

Animals↗

PubMedDate not supplied

[Evaluation of the effect of medicines on biological properties of Clostridium difficile].

The presence of the persistence factors (anti-lysozyme and anti-complement activity) in the vegetative forms of C. difficile was experimentally proved. The effect of different medicines (vitamins B1, B6 and C, prebiotic inulin, probiotics Bifidumbacterin and Enterol) on the persistence factors of C. difficile and microbial resistance to vancomycin, thienam, lincomycin, clindamycin was evaluated. The anti-lysozyme and anti-complement activity of C. difficile was found to decrease under the influence of vitamins B1, B6, C, inulin, exometabolites of bifidobacteria. Under the impact of the preparations used in this study changes in the sensitivity of C. difficile to antibiotics of the lincoamide, carbapenem, glycopeptide groups were found to occur. The data obtained reveal one of the possible mechanisms of the corrective action of the medicines under study on the intestinal microbiocenosis in patients with antibiotic-associated colitis.

Anti-Bacterial Agents↗

PubMed1992

Antimicrobial susceptibility of Clostridium difficile strains isolated from hospitalised patients with acute diarrhoea.

The susceptibility of 43 Clostridium difficile strains to twelve antimicrobials was tested in vitro by agar dilution. All of the 43 strains were inhibited by low concentrations of metronidazole, penicillin G, tetracycline and ampicillin. The strains were highly resistant to gentamycin, trimethoprim, sulphamethoxazole, nalidixic acid, cycloserine, cefotaxime and uniformly sensitive to metronidazole and penicillin G whereas the activity of other antimicrobials are variable.

Acute Disease↗

PubMed1992

Typing of toxic strains of Clostridium difficile using DNA fingerprints generated with arbitrary polymerase chain reaction primers.

Clostridium difficile is the causative agent for pseudomembranous colitis in humans. Toxic strains of C. difficile produce two toxins, toxin A and toxin B. A reliable and definitive method of typing the toxic strains of C. difficile is needed since nosocomial cross infection is a primary concern in hospitals and other health care facilities. A method for typing toxic strains of Clostridium difficile using arbitrary polymerase chain reaction (PCR) primers is presented in this study. The C. difficile strains were initially characterized for the toxin A genetic determinant using specific PCR primers which differentiate toxin positive from toxin negative strains. These toxic strains were then PCR typed using six arbitrary primers which generated DNA patterns that were unique for all toxic strains examined. The use of this typing scheme in clinical applications is discussed.

Bacterial Typing Techniques↗

PubMed1994

Clostridium difficile colonization and diarrhea at a tertiary care hospital.

Clostridium difficile is the major identifiable infectious cause of nosocomial diarrhea. A prospective study was conducted at New England Deaconess Hospital (Boston) to examine risk factors for C. difficile carriage at both admission and follow-up. Specimens from patients admitted to two wards (one medical, one surgical) and three intensive care units (two surgical, one medical) were cultured weekly until discharge. For 89 (18%) of 496 patient admissions, at least one culture was positive. The prevalence of culture positivity within 72 hours of admission was 11%. Risk factors for culture positivity at admission were prior C. difficile diarrhea (adjusted odds ratio [OR] = 9.5), renal insufficiency (OR = 6.7), and recent hospitalization elsewhere (OR = 3.1). Fifteen percent of patients for whom initial cultures were negative and for whom follow-up cultures were performed acquired C. difficile. Admission to the vascular surgery service (relative risk [RR] = 2.3) and liver transplantation (RR = 4.2) were significant risk factors for C. difficile acquisition. Patients asymptomatically colonized on admission had very low risk (1 in 44) for subsequent development of C. difficile diarrhea. In contrast, nine (47%) of 19 patients who acquired toxigenic strains developed C. difficile diarrhea, a finding suggesting that progression to diarrhea occurs early after acquisition or does not occur at all. The relatively high prevalence of culture positivity at admission may be characteristic of tertiary care hospitals and adds to the difficulty of controlling this nosocomial pathogen.

Aged↗

PubMed1998

Clostridium difficile associated with acute colitis in mares when their foals are treated with erythromycin and rifampicin for Rhodococcus equi pneumonia.

In Sweden, mares sometimes develop acute, often fatal, colitis when their foals are treated orally with erythromycin and rifampicin for Rhodococcus (R.) equi infection. Clostridium (C.) difficile, or its cytotoxin, was demonstrated in faecal samples from 5 of 11 (45%) mares with diarrhoea. By contrast C. difficile was not found in the faecal flora of 12 healthy mares with foals treated for R. equi infection or in 56 healthy mares with healthy untreated foals. No other enteric pathogen was isolated from any diarrhoeic mare. Of 7 investigated treated foals, 4 had a high (1651.0, 1468.3, 273.0 and 88.8 microg/g) faecal concentration of erythromycin. The dams of those 4 foals developed acute colitis, whereas the dams of 3 foals with a lower (26.3, 4.6 and 3.7 microg/g) faecal erythromycin concentration remained healthy, indicating that there might have been an accidental intake of erythromycin by mares. The foals treated with antibiotics were regarded as asymptomatic carriers and potential reservoirs, as C. difficile was found in 7 of 16 foals investigated, while 56 untreated foals proved negative. The isolated C. difficile strains proved resistant to both erythromycin (MIC>256 mg/l) and rifampicin (MIC>32 mg/l), a fact that may have favoured the growth of C. difficile in the foal intestine. All mares found positive for C. difficile were, or had recently been, hospitalised together with their foals, indicating that C. difficile may be a nosocomial infection, in horses. The results emphasise that routine testing for C. difficile and its cytotoxin is recommended when acute colitis occurs in mares when their foals are treated with erythromycin and rifampicin. Preventive measures in order to avoid accidental ingestion of erythromycin by mares from the treatment of their foals are suggested.

Actinomycetales Infections↗

PubMed2006

Antimicrobial susceptibility pattern of Clostridium difficile and its relation to PCR ribotypes in a Swedish university hospital.

All 238 Clostridium difficile isolates were susceptible to metronidazole and vancomycin, whereas 84% and 1% were resistant to clindamycin and fusidic acid. Etest MICs for metronidazole were lower than agar dilution MICs (P < 0.01) but without difference in susceptible-intermediate-resistant categorization. No particular PCR ribotype was associated with clindamycin or fusidic acid resistance.

Anti-Bacterial Agents↗

PubMed1993

Comparison of typing methods for Clostridium difficile isolates.

A simple discriminative typing method for Clostridium difficile has been developed. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of whole-cell proteins and restriction enzyme analysis are relatively simple techniques but are difficult to evaluate, especially the restriction enzyme analysis. Immunoblotting and restriction fragment length polymorphism typing facilitate simple discrimination of patterns.

Bacterial Typing Techniques↗

PubMed1993

Detection of toxigenic Clostridium difficile in fecal samples by colony blot hybridization.

A hybridization assay for detection of toxigenic Clostridium difficile in fecal samples was developed and compared with the classical tissue culture cytotoxicity assay. A DNA fragment probe specific for the toxin B gene of Clostridium difficile was synthesized by the polymerase chain reaction and labelled with digoxigenin. Fecal samples were cultured for 24 hours, replica-plated and hybridized with the probe. The hybridization assay had a sensitivity of 100%, specificity of 96.7%, positive predictive value of 86.7% and negative predictive value of 100% compared with the cytotoxicity assay.

Base Sequence↗

PubMed2000

Evaluation of the clinical usefulness of C. difficile toxin testing in hospitalized patients with diarrhea.

Although numerous studies have evaluated the sensitivity and specificity of different assays for Clostridium difficile toxin, none has evaluated how physicians utilize these tests or respond to test results. Therefore, we assessed patient characteristics, clinical findings, and physician responses to positive and negative assay results at two university-affiliated hospitals, one of which used a cell cytotoxicity assay to test for C. difficile toxin and the other of which used an enzyme immunoassay. Two hundred one patient samples at Hospital A and 199 samples at Hospital B were assessed. Positive toxin assays were more frequent at Hospital A than at Hospital B (p < 0.001), at least in part due to the fact that patients tested at Hospital A were more likely to have fever (p < 0.001), an abnormal abdominal exam (p < 0.001), an abnormal leukocyte count (p < 0.001), and a history of prior antibiotic use (p < 0.001). Empiric therapy for C. difficile before results of the toxin assay was more common (p < 0.001) at Hospital A (83/201, 41. 3%) than at Hospital B (25/199, 12.5%). Once empiric therapy was started, most physicians continued therapy despite negative test results (Hospital A, 76%; Hospital B, 69%). Patients who were treated empirically were more likely than patients not treated empirically to have positive toxin assay results and to have fever (p < 0.001), an abnormal abdominal exam (p = 0.003), or an abnormal leukocyte count (p < 0.05). Physicians seldom ordered repeat toxin assays (Hospital A, 14%; Hospital B, 10%) if the initial assay result was negative. In logistic regression analysis, predictors of a positive toxin assay were prior antibiotic therapy, an abnormal abdominal exam, residence at Hospital A, and age >/= 60 years. Predictors of empiric therapy were residence at Hospital A and prior antibiotic therapy. Because physicians electing to empirically treat inpatients with diarrhea rarely alter therapy based on C. difficile toxin assay results, a more cost-effective management strategy may be not to obtain a toxin assay at all in such situations. Testing should be limited to patients who have received antibiotics within the prior month and who have significant diarrhea and/or abdominal pain.

Bacterial Toxins↗

PubMed2001

Probiotic activities of Lactobacillus casei rhamnosus: in vitro adherence to intestinal cells and antimicrobial properties.

The interest of probiotics as remedies for a broad number of gastrointestinal and other infectious diseases has gained wide interest over the last few years, but little is known about their underlying mechanism of action. In this study, the probiotic activities of a human isolate of Lactobacillus casei subsp. rhamnosus strain (Lcr35) were investigated. Using intestinal Caco-2 cell line in an in vitro model, we demonstrated that this strain exhibited adhesive properties. The inhibitory effects of Lcr35 organisms on the adherence of three pathogens, enteropathogenic Escherichia coli (EPEC), enterotoxigenic E. coli (ETEC) and Klebsiella pneumoniae, were determined. A decrease in the number of adhering pathogens was observed, using either preincubation, postincubation or coincubation of the pathogens with Lcr35. Moreover, the antibacterial activities of cell-free Lcr35 supernatant was examined against nine human pathogenic bacteria, ETEC, EPEC, K. pneumoniae, Shigella flexneri, Salmonella typhimurium, Enterobacter cloacae, Pseudomonas aeruginosa, Enterococcus faecalis and Clostridium difficile. The growth of all strains was inhibited, as measured by determining the number of viable bacteria over time, but no bactericidal activity was detected in this in vitro assay. Together, these findings suggest that this probiotic strain could be used to prevent colonization of the gastrointestinal tract by a large variety of pathogens.

Antibiosis↗

PubMed2005

A predominantly clonal multi-institutional outbreak of Clostridium difficile-associated diarrhea with high morbidity and mortality.

BACKGROUND: In March 2003, several hospitals in Quebec, Canada, noted a marked increase in the incidence of Clostridium difficile-associated diarrhea. METHODS: In 2004 we conducted a prospective study at 12 Quebec hospitals to determine the incidence of nosocomial C. difficile-associated diarrhea and its complications and a case-control study to identify risk factors for the disease. Isolates of C. difficile were typed by pulsed-field gel electrophoresis and analyzed for binary toxin genes and partial deletions in the toxin A and B repressor gene tcdC. Antimicrobial susceptibility was evaluated in a subgroup of isolates. RESULTS: A total of 1703 patients with 1719 episodes of nosocomial C. difficile-associated diarrhea were identified. The incidence was 22.5 per 1000 admissions. The 30-day attributable mortality rate was 6.9 percent. Case patients were more likely than matched controls to have received fluoroquinolones (odds ratio, 3.9; 95 percent confidence interval, 2.3 to 6.6) or cephalosporins (odds ratio, 3.8; 95 percent confidence interval, 2.2 to 6.6). A predominant strain, resistant to fluoroquinolones, was found in 129 of 157 isolates (82.2 percent), and the binary toxin genes and partial deletions in the tcdC gene were present in 132 isolates (84.1 percent). CONCLUSIONS: A strain of C. difficile that was resistant to fluoroquinolones and had binary toxin and a partial deletion of the tcdC gene was responsible for this outbreak of C. difficile-associated diarrhea. Exposure to fluoroquinolones or cephalosporins was a risk factor.

Aged↗

PubMed1991

Time-dependent killing of Clostridium difficile by metronidazole and vancomycin.

Killing of Clostridium difficile by metronidazole and vancomycin was studied with a batch culture method. Pre-reduced 50 ml volumes of brain heart infusion broth containing one of a range of concentrations of either vancomycin or metronidazole were inoculated with approximately 10(6) cfu/ml of C. difficile. The cultures were incubated anaerobically at 35 degrees C for 24 h. Total viable counts and spore counts were performed with a modified Miles and Misra technique. Concentrations of metronidazole and vancomycin below the respective MICs had no effect on the growth of C. difficile. A significant reduction in numbers of vegetative cells and spores occurred in the presence of concentrations of both agents close to their respective MICs. A bacteriostatic effect was observed when vancomycin concentrations similar to those occurring in faeces following oral administration of the drug were used. In contrast, rapid killing of vegetative cells occurred over a wide range of metronidazole concentrations greater than the MIC.

Clostridioides difficile↗

PubMed1994

Cloning of a genetic determinant from Clostridium difficile involved in adherence to tissue culture cells and mucus.

Our laboratory has previously shown that Clostridium difficile adherence to Caco-2 cells is greatly enhanced after heat shock at 60 degrees C and that it is mediated by a proteinaceous surface component. The experiments described here show that C. difficile could adhere to several types of tissue culture cells (Vero, HeLa, and KB) after heat shock. The type of culture medium (liquid or solid, with or without blood) had little effect on adhesion. To clone the adhesin gene, polyclonal antibodies against C. difficile heated at 60 degrees C were used to screen a genomic library of C. difficile constructed in lambda ZapII. Ten positive clones were identified in the library, one of which (pCL6) agglutinated several types of erythrocytes in the presence of mannose. In Western blots (immunoblots), this clone expressed in Escherichia coli a 40- and a 27-kDa protein; a 27-kDa protein has been previously identified in the surface extracts of heat-shocked C. difficile as a possible adhesin. The clone adhered to Vero, Caco-2, KB, and HeLa cells; the adherence was blocked by anti-C. difficile antibodies, by a surface extract of C. difficile, and by mucus isolated from axenic mice. Furthermore, the clone could attach ex vivo to intestinal mucus isolated from axenic mice. Preliminary studies on the receptor moieties implicated in C. difficile adhesion revealed that glucose and galactose could partially block adhesion to tissue culture cells, as did di- or trisaccharides containing these sugars, suggesting that the adhesin is a lectin. In addition, N-acetylgalactosamine, a component of mucus, and gelatin partially impeded cell attachment.

Animals↗

PubMed1996

Effect of Clostridium difficile toxin A on human intestinal epithelial cells: induction of interleukin 8 production and apoptosis after cell detachment.

Clostridium difficile is the aetiological agent of pseudomembranous colitis, and animal studies suggest the essential role of secreted toxin A in inducing disease. This study examined the biological responses to toxin A by human intestinal epithelial cells. Confluent monolayers of Caco2, HT29, and T84 cells and primary epithelial cells in organ cultures of human colonic biopsy specimens and after detachment with EDTA were studied. Interleukin 8 was assayed using enzyme linked immunosorbent assay (ELISA). Purified C difficile toxin A induced cell rounding and detachment of monolayers of the epithelial cell lines. Cells in detached monolayers initially remained viable while adherent to each other. Subsequently, an increasing number of apoptotic cells appeared in suspension. Exposure to toxin A for 24 hours induced interleukin 8 production in T84 and HT29 cells. Toxin A also induced epithelial cell rounding, detachment, and apoptosis in organ cultures of human colonic biopsy specimens. During culture (in medium only), EDTA detached colonic epithelial cells produced interleukin 8 and cell death occurred by apoptosis. Colonic disease by C difficile may be initiated by toxin A mediated induction of epithelial cell interleukin 8 production and apoptosis after cell detachment from the basement membrane. Studies on isolated (toxin untreated) colonic epithelial cells suggest that interleukin 8 production and apoptosis occur as a consequence of cell injury and detachment.

Apoptosis↗

PubMed2001

Clostridium difficile colitis following antibiotic prophylaxis for dental procedures.

Clostridium difficile-induced diarrhea and colitis are common complications of therapeutic courses of antibiotics in the hospital setting. We report a case of Clostridium difficile colitis following antibiotic prophylaxis for endocarditis prior to dental procedures in the community setting. The infection necessitated hospital admission and a prolonged hospital stay. Dental practitioners must be aware of the significance of the disease and the risk associated with antibiotics, whether they are used for prophylaxis or treatment.

Aged↗

PubMed2002

[Antibiotic induced diarrhea and pseudomembranous colitis].

The spore-forming anaerobic bacterium Clostridium difficile has become a serious enteropathogen. Oral and parenteral administration of antibiotics can cause ecological disturbances in the normal intestinal microflora. Suppression of the normal microflora may lead to reduced colonization resistance with subsequent overgrowth by pre-existing, naturally resistant microorganisms, such as C. difficile. C. difficile infection shows a range of clinical presentations between an asymptomatic carrier state, light diarrhea without inflammatory changes, and pseudomembranous colitis. C. difficile infection is acquired by the fecal-oral or environmental-oral routes. From March 2000 through March 2001 we assessed 48 cases of nosocomial antibiotic-associated diarrhea (AAD). Of these, 21 were due to C. difficile (CDAD). Cephalosporin was the agent most commonly associated with CDAD. Avoidance of cephalosporins, strict use of "single shot" prophylaxis, isolation of infected, symptomatic patients in single-bed rooms, improved hygiene and complete room disinfection lead to a rapid decrease of CDAD. The etiology, prognosis and prophylaxis are discussed in this paper.

Aged↗

PubMed1998

Multicentre evaluation of a commercial test for the rapid diagnosis of Clostridium difficile-mediated antibiotic-associated diarrhoea.

An immunoassay for the detection of Clostridium difficile toxin A in stool samples (Clearview C. DIFF A; Unipath, UK) was evaluated against the cell cytotoxicity assay using 407 stool samples from patients suspected to have, or considered at risk of, antibiotic-associated diarrhoea. Of the samples tested, 98 were positive and 280 were negative by both tests (sensitivity 83.1%, specificity 96.9%). Following resolution of the 29 discrepant results, the sensitivity and specificity of the immunoassay were 91% and 98%, respectively, and the sensitivity for the cell cytotoxicity assay was calculated as 91.5%, with a specificity of 99%. The Clearview C. DIFF A test proved to be a rapid simple assay for the detection of Clostridium difficile toxin A in stool samples. The test was equally suited to single or batch testing, required minimal sample handling, and provided results within 30 min of applying the sample to the test unit.

Animals↗