First isolation of Clostridium difficile PCR ribotype 027, toxinotype III in Belgium.
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First isolation of Clostridium difficile PCR ribotype 027 in Austria.
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The spectrum of pseudomembranous enterocolitis and antibiotic-associated diarrhea.
Pseudomembranous (entero)colitis is primarily caused by Clostridium difficile infection. The most common predisposing factor is prior use of antibiotics, including vancomycin and metronidazole, which themselves are therapy for C difficile colitis. Other risk factors have also been described. The presence of C difficile in the gastrointestinal tract leads to a spectrum of manifestations from the asymptomatic carrier state to fulminant colitis. Successful treatment of C difficile colitis requires prompt treatment with appropriate antibiotics, withdrawal of the suspected predisposing antibiotics, and, in rare cases, total colectomy. Preventive measures of adequate infection control and judicious use of antibiotics are necessary means in attempting to control the spread of C difficile infection. Attempts at making an effective human vaccine are currently under way.
Anti-Bacterial Agents↗
Chronic septic arthritis and osteomyelitis in a prosthetic knee joint due to Clostridium difficile.
A case of chronic septic arthritis and osteomyelitis in a prosthetic knee joint due to Clostridium difficile is reported. A knee prosthesis was installed in a 16-year-old boy for surgical treatment of an osteosarcoma of the femur. Later, the patient suffered a traumatic closed fracture of his patella, and a sterile fluid was aspirated. One month later, the joint displayed inflammation. Culture of the articular fluid yielded a nontoxigenic Clostridium difficile strain. Despite several attempts using conservative medical treatment with penicillins and ornidazole, Clostridium difficile strains with the same antibiotic susceptibility pattern were repeatedly isolated from the joint over an eight-month period. The foreign material was then ablated, and finally, the patient's leg was amputated one year after Clostridium difficile was first isolated. The possible sources of contamination in our case and other reported cases of extraintestinal infection due to Clostridium difficile are discussed.
Adolescent↗
Limited clinical utility of Clostridium difficile toxin testing in infants in a pediatric hospital.
Previous studies have shown high rates of asymptomatic carriage of toxin-producing Clostridium difficile in infants. We performed a retrospective case control study comparing infants younger than 1 year old with diarrhea and C. difficile toxin (CDT) in the stool, to age-matched controls with diarrhea lacking CDT in the stool. We found no difference in clinical characteristics including fever, vomiting, or hematochezia. Treatment with metronidazole had no significant effect on the clinical outcome. Alternative etiologies for diarrhea (most commonly viral) were found in more than 50% of patients in both groups. We recommend that other causes of diarrhea be considered before C. difficile colitis in this age group.
Anti-Infective Agents↗
The effect of probiotics on Clostridium difficile diarrhea.
Clostridium difficile is the leading cause of nosocomially acquired intestinal infection in the United States, affecting virtually all cases of pseudomembranous colitis and up to 20% of cases of antibiotic-associated diarrhea. Even after receiving antibiotic treatment with either metronidazole or vancomycin, 20% of patients will have recurrent Clostridium difficile diarrhea. An innovative approach to the problem involves the introduction of competing, nonpathogenic (probiotic) organisms into the intestinal tract to restore microbial balance. The theoretical premise behind this approach is that the protective intestinal microflora is damaged by antibiotic treatment; the initial antibiotic exposure thus leaves the host susceptible to colonization and subsequent infection by Clostridium difficile. A so-called "second-hit" to the intestinal microflora occurs when the infected host is treated with flagyl or vancomycin, further destroying susceptible bacterial flora. Probiotic agents, such as Lactobacillus GG and Saccharomyces boulardii, have been studied for the treatment of Clostridium difficile. We are currently running a prospective, randomized, placebo-controlled trial of Lactobacillus GG in combination with standard antibiotics for the treatment of Clostridium difficile infection. Although it is too early to draw statistically significant conclusions, two patterns seem to be emerging: Lactobacillus GG is effective in reducing the 3-wk recurrence rate of Clostridium difficile, and patients feel better when taking Lactobacillus GG, as compared with the placebo, with early disappearance of abdominal cramps and diarrhea. In conclusion, the use of probiotics for the treatment of primary and recurrent Clostridium difficile diarrhea looks promising. Patients seem to have less recurrent Clostridium difficile diarrhea and early symptomatic improvement when using the probiotic Lactobacillus GG.
Aged↗
Arbitrary primed PCR rules out Clostridium difficile cross-infection among patients in a haematology unit.
Eight out of 20 (40%) patients with haematological malignancies hospitalized in the same unit of our hospital from 24 January to 24 April 1995, suffered from diarrhoea due to Clostridium difficile. The C. difficile isolates were characterized by serotyping and by arbitrary primed polymerase chain reaction (AP-PCR) using three different 10-mer oligonucleotides. It was found by serotyping that five patients had non-typeable isolates and three had serogroup H isolates. The AP-PCR typed all the isolates and yielded various patterns suggesting that there had been no cross-transmission between the patients. Control faecal sample cultures showed that two patients were still carrying the same isolates after specific treatment with vancomycin or metronidazole, and that one patient had acquired an isolate with a new AP-PCR type. AP-PCR was found to be a rapid, effective discriminative method for the immediate epidemiological tracking of hospital-acquired infections due to C difficile.
Adult↗
Association of IgA nephropathy with Clostridium difficile colitis.
Immunoglobulin A (IgA) nephropathy, the most common cause of glomerulonephritis worldwide, is usually idiopathic in origin and renal limited. Secondary IgA nephropathy has been associated with systemic disease, including such gastrointestinal tract disturbances as celiac sprue and inflammatory bowel disease. We describe gross hematuria and reversible acute renal failure from IgA nephropathy in a patient with cephalosporin-induced Clostridium difficile colitis. In addition to mesangial IgA and C3 deposition, renal histological examination showed glomerular bleeding, intratubular red blood cell casts, and acute tubular necrosis. To the best of our knowledge, this is the first report of an association between IgA nephropathy and C difficile colitis.
Acute Kidney Injury↗
Inactivation of Clostridium difficile spores by disinfectants.
OBJECTIVE: The current study was designed to evaluate the activity of glutaraldehyde-based disinfectants against Clostridium difficile using the Association of Official Analytical Chemists' (AOAC) sporicidal test. This study was undertaken because gastrointestinal endoscopes that may be contaminated with C difficile spores are most commonly disinfected between patients using glutaraldehyde-based disinfectants. DESIGN: Using the AOAC test, the following disinfectants were tested: 2% alkaline glutaraldehyde, 2% acid glutaraldehyde, a 1:16 dilution of a 2% glutaraldehyde-7.05% phenol-1.20% sodium phenate, and a 1:20 dilution of a 10% glutaraldehyde-0.5% phenylphenol-0.1% amylphenol. RESULTS: Test results of the four disinfectants against C difficile spores at exposure times of 10, 20, and 60 minutes were as follows (number of positive penicylinders per 30 replicates): 0, 0, and 0 for 2% alkaline glutaraldehyde; 6, 3, and 0 for 2% acid glutaraldehyde; 30, 29, and 30 for a 1:16 dilution of glutaraldehyde-7.05% phenol-1.20% sodium phenate; and 30, 30, and 30 for a 1:20 dilution of glutaraldehyde-0.5% phenylphenol-0.1% amylphenol. CONCLUSIONS: C difficile spores are more susceptible to inactivation by glutaraldehyde-based disinfectants than the spore-forming organisms recommended in the AOAC sporicidal test (i.e., Bacillus subtilis and Clostridium sporogenes). Diluting glutaraldehyde-based disinfectants below 2% led to the inability to inactivate spores of C difficile using exposure times commonly employed to disinfect semicritical items such as gastrointestinal endoscopes.
Clostridioides difficile↗
Antimicrobial susceptibility of equine and environmental isolates of Clostridium difficile.
The antimicrobial susceptibility of 50 Clostridium difficile isolates, 36 of them from horse feces and 14 from environmental sites, was determined by broth microdilution. The antimicrobial agents tested were avilamycin, cephalothin, chloramphenicol, clindamycin, erythromycin, gentamicin, neomycin, oxacillin, oxytetracycline, penicillin, spiramycin, streptomycin, trimethoprim/sulfamethoxazole, vancomycin, and virginiamycin. All isolates were susceptible to vancomycin (MIC </=1 microg/ml). The MICs of erythromycin, oxytetracycline, spiramycin, and virginiamycin showed a bimodal distribution. Compared with the majority of isolates, the MICs of erythromycin (MIC > 16 microg/ml), oxytetracycline (MIC >/=32 microg/ml), spiramycin (MIC > 16 microg/ml), and virginiamycin (MIC 8-16 microg/ml) were higher for 18 isolates. Those were mainly isolated from horses at animal hospitals and further from environmental sites at a stud farm. In contrast, all isolates, except one, from healthy foals had low MICs of erythromycin, spiramycin, virginiamycin, and oxytetracycline. The isolates from soil in public parks had also low MICs of these antimicrobial agents. Broth microdilution appeared both reliable and reproducible for susceptibility testing of C. difficile. The method was also readily performed and the MIC endpoints were easily read.
Animals↗
Effects of cefotaxime and desacetylcefotaxime upon Clostridium difficile proliferation and toxin production in a triple-stage chemostat model of the human gut.
Clostridium difficile is recognized as an important nosocomial pathogen. C. difficile infection (CDI) is thought to arise as a result of depletion of the normal gut flora by antimicrobial agents. Cefotaxime (CTX) is well-known for its propensity to cause CDI, but the reasons behind its particular predisposition to the disease remain unclear. Previous investigations have so far relied upon the hamster model of CDI or human volunteers. We have used a triple-stage chemostat model of the human gut to investigate the behaviour of C. difficile and components of the normal gut flora, in response to exposure to CTX alone, and in combination with its active metabolite desacetylcefotaxime (dCTX). C. difficile remained in a steady state during non-antibiotic exposed periods, with no detectable cytotoxin. During both antibiotic exposure regimens, proliferation of C. difficile and elevated cytotoxin levels were observed. Cessation of antibiotic instillation produced a reduction in cytotoxin levels and viable counts. Decreases in bacterial counts were observed in response to both antibiotic exposure regimens, notably for bifidobacteria and bacteroides. Numbers of bacteroides were profoundly affected by exposure to the CTX/dCTX combination, and this may indicate a possible role for bacteroides in colonization resistance. We believe that the gut model is a promising method for studying C. difficile pathogenesis in conditions analogous to the in vivo situation.
Bacterial Toxins↗
Effects of piperacillin/tazobactam on Clostridium difficile growth and toxin production in a human gut model.
OBJECTIVES: Clostridium difficile infection (CDI) is a major cause of morbidity in the nosocomial environment. Antimicrobial agents such as the third-generation cephalosporins, lincosamides and aminopenicillins are well known for their propensity to induce CDI, but the definitive reasons why remain to be elucidated. Despite their broad spectrum of activity against both aerobic and anaerobic bacteria, the ureidopenicillins remain a class of antimicrobials infrequently associated with the development of CDI. METHODS: We used a triple-stage chemostat model that simulates the human gut to study the effects of the ureidopenicillin/beta-lactamase inhibitor combination piperacillin/tazobactam on gut bacterial populations and C. difficile. RESULTS: Piperacillin/tazobactam rapidly reduced all enumerated gut bacterial populations (including bacteroides, bifidobacteria and lactobacilli) below the limits of detection by the end of the piperacillin/tazobactam instillation period. Despite such widespread disruption of gut bacterial populations, C. difficile populations remained principally as spores, with no sustained proliferation or high-level cytotoxin production observed. CONCLUSIONS: Factors other than reduced colonization resistance must be responsible for determining whether CDI develops following antimicrobial administration. We believe the gut model is a promising approach for the study of C. difficile pathogenesis reflecting in vivo events likely to occur in CDI.
Anti-Bacterial Agents↗
Tigecycline does not induce proliferation or cytotoxin production by epidemic Clostridium difficile strains in a human gut model.
OBJECTIVES: Data on the risk of Clostridium difficile infection (CDI) associated with specific antibiotics are difficult to obtain because of confounding clinical factors. It is particularly important to evaluate the propensity of new antibiotics to induce CDI. We have examined the propensity of tigecycline to induce CDI using a human gut model. METHODS: We used a three-stage chemostat human gut model to study the effects of tigecycline on indigenous gut microflora and C. difficile. Two epidemic C. difficile were studied in separate experiments: PCR ribotype 001 (UK, CD001) and PCR ribotype 027 (North America, CD027). Tigecycline MICs for 39 C. difficile representing 19 distinct PCR ribotypes were also determined. RESULTS: Tigecycline MICs were 0.06 mg/L for all the C. difficile strains. Peak tigecycline concentrations in the gut model were 10.9 and 11.7 mg/L in CD027 and CD001 experiments, respectively. Tigecycline instillation invoked marked decreases in numbers of bacteroides and bifidobacteria (10(7)-10(8) cfu/mL) and lesser reductions in facultative anaerobes. Despite markedly altered gut microflora, CD001 and CD027 remained as spores for the duration of the experiment, with no evidence of proliferation or cytotoxin production. CONCLUSIONS: Tigecycline exposure did not induce C. difficile proliferation or cytotoxin production despite reduced competing microflora. The potency of tigecycline against C. difficile may contribute to the low risk of CDI induction. Factors other than gut microflora colonization resistance may be important in preventing C. difficile spore germination, proliferation and cytotoxin production.
Anti-Bacterial Agents↗
Flow cytometric analysis of Clostridium difficile adherence to human intestinal epithelial cells.
Clostridium difficile is the most common cause of diarrhoea in hospitalised patients. Bacterial adherence to gut epithelial cells is a likely prerequisite to infection and toxin production. A novel flow cytometric method was developed for detecting adherence of C. difficile to human colonic and small intestinal epithelial cells (EC) and human intestinal cell lines. Small intestinal and colonic EC were isolated from biopsy specimens with mucolytic and chelating agents. Adherence of fluorochrome-labelled C. difficile to EC was measured by flow cytometry and was calculated as increase in median fluorescent intensity (deltaMFI). Cells with bacteria attached could be distinguished easily from cells alone or cells with unlabelled bacteria attached. Toxin-positive C. difficile adhered to colonic and small intestinal EC (deltaMFI mean 21.2 SD 16.7, n = 33 and 16.5 SD 20.7, n = 19 respectively). The toxin-negative strain also adhered to both epithelial cell types (deltaMFI 26.1 SD 32.5, n = 17 and 18.3 SD 31.3, n = 16). Adherence of toxin-positive C. difficile to the intestinal cell lines Caco-2 (deltaMFI 9.4 SD 4.4, n = 14) and HT29 (deltaMFI 8.1 SD 3.1, n = 12) was quantifiable, although at a significantly lower level than with primary colonic epithelial cells. Adherence of the toxin-negative strain was slightly lower, deltaMFI 6.5 SD 1.8, n = 9 with Caco-2 cells and deltaMFI 6.0 SD 2.0, n = 10 with HT29 cells. Adherence of C. difficile to epithelial cell lines was blocked with C. difficile antiserum, confirming specificity of adherence. In conclusion, flow cytometry is a useful approach to quantifying adherence of C. difficile to human colonic and small intestinal epithelial cells. Binding of toxin-negative as well as toxin-positive bacteria was detectable by this approach. Analysis of C. difficile adherence to target cells may have important implications for the understanding of the pathogenesis of C. difficile-related disease.
Bacterial Adhesion↗
Characterisation of Clostridium difficile strains by polymerase chain reaction with toxin A- and B-specific primers.
A total of 218 Clostridium difficile strains was examined for production of toxin A by ELISA, production of toxin B by a cytotoxin assay and the presence of toxin A and B gene-associated sequences by the polymerase chain reaction (PCR). After saturation amplification with toxin B-specific primers, the characteristic amplification product (591 bp) was detected in all 184 toxigenic strains examined. PCR with toxin A-specific primers gave positive results with all but one of the toxigenic strains. By contrast, PCR with toxin A- and toxin B-specific primers yielded negative results with all 34 non-toxigenic strains tested. This suggests that PCR detection of either the toxin A or B gene is a good indication of toxin production. PCR did not require DNA extraction or hybridisation and was convenient, sensitive and rapid. Toxigenic C. difficile could be detected in mixed cultures, suggesting a role for PCR in the identification of toxigenic C. difficile in primary culture.
Bacterial Proteins↗
Distribution of Clostridium difficile variant toxinotypes and strains with binary toxin genes among clinical isolates in an American hospital.
Genetic variants of Clostridium difficile have been reported with increasing frequency, but their true incidence is unknown. C. difficile strains have been classified into variant toxinotypes according to variations in the pathogenicity locus encoding the major virulence factors, toxins A and B. Some strains produce an additional toxin, binary toxin CDT. This survey of clinical isolates (153) from patients in a single hospital set out to ascertain the distribution of variant toxinotypes and strains possessing binary toxin genes. A PCR-RFLP-based method of toxinotyping identified 123 (80.4 %) isolates as toxinotype 0, 13 (8.5 %) strains as non-toxigenic and 17 (11.1 %) as belonging to variant toxinotypes. Binary toxin genes were amplified by PCR in nine strains (5.8 %), all of which were variant toxinotypes. Toxin variants of C. difficile are pathogenic and commonly isolated and need to be considered when evaluating new diagnostic testing strategies for C. difficile disease.
ADP Ribose Transferases↗
[A nosocomial outbreak of diarrhea caused by toxin A-negative, toxin B-positive Clostridium difficile in a cancer center hospital].
Between February and July 2001, 15 patients were diagnosed as Clostridium difficile-associated diarrhea in a ward of hematological neoplasm and lung cancer in a cancer center hospital. Of these 15 patients, 10 had malignant lymphoma, and 12 and 11 had exposure to antimicrobial agents and cancer chemotherapy, respectively, before the onset of diarrhea. Toxin A-positive, toxin B-positive (A+ B+) C. difficile was recovered from five patients and the remaining 10 patients suffered from diarrhea caused by toxin A-negative, toxin B-positive (A- B+) strains. All of the 10A- B+ isolates represented an identical banding pattern by PCR ribotyping and classified into one type (two subtypes) by pulsed field gel electrophoresis typing, indicating that a nosocomial outbreak of diarrhea caused by A- B+ C. difficile occurred among the patients hospitalized on this ward. Detection of toxin A in stool specimens by a toxin A detection kit was performed on 14 patients. Although two patients who carried A+ B+ strains were positive for toxin A assay, toxin A detection test was negative in 12 patients including 10 patients with A- B+ C. difficile infection. Diagnosis of C. difficile-associated diarrhea by combination of toxin A assay in feces and culture of C. difficile could successfully lead to recognition of an outbreak caused by A- B+ C. difficile in a cancer center hospital.
Adult↗
Isolation of RNA polymerase from Clostridium difficile and characterization of glutamate dehydrogenase and rRNA gene promoters in vitro and in vivo.
Clostridium difficile is the primary causative agent of antibiotic-associated diarrheal disease. To facilitate molecular genetic analysis of gene expression in this organism, methods were developed to study transcriptional regulation in vitro and in vivo. That is, C. difficile RNA polymerase was partially purified and shown to bind to and initiate transcription in vitro from bona fide C. difficile promoters for rRNA and glutamate dehydrogenase genes. In addition, primer extension analyses and a beta-glucuronidase reporter system were used to quantitate transcription from these promoters in vivo. With these tools in hand, it is now possible to characterize the behavior of any C. difficile gene in vivo and to study the regulation of its expression in detail.
Base Sequence↗