Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Clostridioides difficile”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,261 records · Page 70Linked to original sources
PubMed2003

Sudden increase of vancomycin-resistant enterococcal infections in a Korean tertiary care hospital: possible consequences of increased use of oral vancomycin.

A sudden increase in vancomycin-resistant enterococci (VRE) infections was noted in 1998 in a tertiary care hospital in Korea. All of the VRE isolated in 1998 in the hospital were VanA type and most were multidrug-resistant Enterococcus faecium. The increase in VRE was probably due to the increased use of oral vancomycin to treat Clostridium difficile infections and clonal as well as horizontal spread. More restricted oral vancomycin use and stricter infection control measures are required to achieve a better control of the spread of VRE.

Administration, Oral↗
PubMed1998

Single toxin detection is inadequate to diagnose Clostridium difficile diarrhea in pediatric patients.

BACKGROUND & AIMS: Clostridium difficile is an important cause of symptomatic diarrhea in pediatric patients. The bacterium produces two toxins, although many laboratories assay for only one. We questioned this diagnostic approach when patients had positive results for C. difficile at our institution, but initially had tested negative at outside laboratories. METHODS: We retrospectively analyzed relative frequencies of C. difficile toxin A alone, toxin B alone, and toxins A and B from pediatric patients with diarrhea. Results were stratified according to toxin detection and patient age. RESULTS: Of 1061 specimens, 276 (26.8%) were positive for C. difficile toxin(s). Fifty-one (18.5%) were positive for toxin A alone, 133 (48.2%) for toxin B alone, and 92 (33.3%) for both toxins. Assaying for toxin B identified C. difficile infection more frequently than did assaying for toxin A (P < 0.0001). The frequency of toxin B detection was significantly higher for older children but not for infants. CONCLUSIONS: Testing for C. difficile toxin A or toxin B alone will result in more frequent misdiagnosis than testing for both toxins. This practice may lead to inappropriate further invasive investigations in children, although this finding may not be applicable to adults.

Adolescent↗
PubMed1996

Financial burden of hospital-acquired Clostridium difficile infection.

Clostridium difficile infection has become endemic in many hospitals and yet few data on the associated costs of such cases are available. We prospectively followed 50 consecutive cases of C. difficile infection and 92 control patients, who were admitted to the same geriatric wards within 72 h of the cases. Cases and controls had similar age, sex and major diagnosis distributions. Cases stayed significantly longer (mean 21.3 days, median 20.5 days; P < 0.001) in hospital than controls, including an average 14 days in a side room. Diarrhoea developed in cases on average 10.8 days after admission, which, when compared with a mean duration of stay for controls of 25.2 days, implies that C. difficile infection caused an increased duration of stay, as opposed to infection occurring because of longer residence. There was a significantly higher death rate in cases compared with controls (P < 0.01). Antibiotic treatment of C. difficile infection cost an average of Pounds 47 per case. The average number of laboratory investigations per day was similar for cases and controls, but the increased length of stay meant an extra cost for tests of approximately Pounds 210 per case. Assuming hotel costs of Pounds 150 (Pounds 200) per day stay (in a side room), 94% of the additional costs associated with C. difficile infection were due to increased duration of stay (Pounds 3850). The total identifiable increased cost of C. difficile infection was, therefore, in excess of Pounds 4000 per case. Such high costs can be used to justify expenditure on personnel and/or other control measures to reduce the incidence of this hospital-acquired infection.

Aged↗
PubMed2002

Epidemiology and outcome of Clostridium difficile infection and diarrhea in HIV infected inpatients.

Clostridium difficile causes diarrhea in HIV infected patients but reports of prevalence, risk factors, and outcome vary. We studied the impact of C. difficile in 161 HIV infected inpatients admitted to Cook County Hospital. Patients with C. difficile had more hospital admissions in the previous 6 months (p =.04), spent more days in the hospital in the previous 3 months (p =.02), more often had previously received H2 blockers or treatment for Pneumocystis carinii (p <.05), and had a more frequent history of herpesvirus (p =.03) or opportunistic infections (p =.04). C. difficile associated diarrhea (CDAD) was the etiology in 32% of all study patients with diarrhea. Patients with CDAD were hospitalized for longer periods (p =.02) and received more antibiotics (p =.002). C. difficile was frequently present in our HIV infected patients, especially those with advanced HIV disease, but appeared to have little impact on morbidity or mortality.

AIDS-Related Opportunistic Infections↗
PubMed2003

Probiotics, antibiotic-associated diarrhoea and Clostridium difficile diarrhoea in humans.

Probiotics are living organisms which, when ingested, have a beneficial therapeutic effect. Examples are bacteria, especially Lactobacillus rhamnosus GG, and the yeast Saccharomyces boulardii. Controlled trials indicate a benefit of both of these in the prevention of antibiotic-associated diarrhoea. Other less effective probiotics are Lactinex, Enterococcus faecium and bifidobacteria. In the difficult clinical problem of recurrent Clostridium difficile disease, S. boulardii as an adjunct to antibiotics has shown benefit in controlled trials. There is, however, less convincing evidence for the efficacy of Lactobacillus GG in this disease. Additional controlled trials and safety studies are needed before there can be a widespread endorsement of probiotics for these two conditions.

Animals↗
PubMed2003

Efficient sporulation in Clostridium difficile requires disruption of the sigmaK gene.

A 14.6 kb prophage-like insertion, termed skinCd, was found to interrupt the sigK gene, which encodes an RNA polymerase sigma factor essential for sporulation, in six strains of Clostridium difficile. Until now, Bacillus subtilis was the only spore-former shown to carry such an insertion, and the presence of the insertion is not required for efficient sporulation in this organism. The B. subtilis and C. difficile skin elements proved to be divergent in sequence, inserted at different sites within the sigK gene and in opposite orientations. The skinCd element was excised from the chromosome specifically during sporulation, forming a circular molecule. Two natural isolates of C. difficile lacked the skinCd element and were defective in sporulation. When a merodiploid strain was created that carries both interrupted and uninterrupted versions of the sigK gene, the cells became Spo-, showing that the uninterrupted gene is dominant and inhibits sporulation. C. difficile sigK genes, whether skinCd+ or skinCd-, lack the N-terminal pro-sequence found in all other sigK genes studied to date. Thus, regulated excision of skinCd appears to be a critical mechanism for achieving proper temporal activation of sigmaK.

Amino Acid Sequence↗
PubMed2003

Mechanism of quinolone resistance in anaerobic bacteria.

Several recently developed quinolones have excellent activity against a broad range of aerobic and anaerobic bacteria and are thus potential drugs for the treatment of serious anaerobic and mixed infections. Resistance to quinolones is increasing worldwide, but is still relatively infrequent among anaerobes. Two main mechanisms, alteration of target enzymes (gyrase and topoisomerase IV) caused by chromosomal mutations in encoding genes, or reduced intracellular accumulation due to increased efflux of the drug, are associated with quinolone resistance. These mechanisms have also been found in anaerobic species. High-level resistance to the newer broad-spectrum quinolones often requires stepwise mutations in target genes. The increasing emergence of resistance among anaerobes may be a consequence of previous widespread use of quinolones, which may have enriched first-step mutants in the intestinal tract. Quinolone resistance in the Bacteroides fragilis group strains is strongly correlated with amino acid substitutions at positions 82 and 86 in GyrA (equivalent to positions 83 and 87 of Escherichia coli). Several studies have indicated that B. fragilis group strains possess efflux pump systems that actively expel quinolones, leading to resistance. DNA gyrase seems also to be the primary target for quinolones in Clostridium difficile, since amino acid substitutions in GyrA and GyrB have been detected in resistant strains. To what extent other mechanisms, such as mutational events in other target genes or alterations in outer-membrane proteins, contribute to resistance among anaerobes needs to be further investigated.

4-Quinolones↗
PubMed1995

Selective neutralization of a bacterial enterotoxin by serum immunoglobulin A in response to mucosal disease.

One-third of convalescent-phase serum samples (6 of 18) from patients with Clostridium difficle-associated diarrhea demonstrated neutralization of the clostridial enterotoxin, toxin A. Although appreciable amounts of toxin A-specific immunoglobulin G (IgG) and IgA were present in these sera, the ability to neutralize the cytotoxic activity of toxin A on OTF9-63 cells in vitro was confined to the IgA fraction and the IgA1 subclass in serum samples from all six patients. In contrast to the patients with C. difficile diarrhea, this activity was present in both the IgA and IgG fractions in sera from two C. difficile-infected patients without diarrhea, one of whom presented with a splenic abscess. Sera and purified IgA which neutralized the cytotoxicity of toxin A on OTF9-63 cell cultures in vitro also neutralized the enterotoxicity of toxin A in rabbit ileal loops in vivo. This activity was not Fc dependent, since IgA retained neutralizing activity after pepsin digestion and F(ab')2 purification. The transition from nonneutralizing toxin A-specific IgA in the acute-phase sera to neutralizing specific IgA in the convalescent-phase sera was accompanied by a shift from a polymeric to a predominantly monomeric form of specific IgA. However, the neutralizing activity in convalescent-phase sera was present as both monomeric and polymeric IgA. Convalescent-phase sera from other patients with C. difficile diarrhea that failed to neutralize toxin A also failed to produce a predominantly monomeric-form specific IgA response. We conclude that serum IgA, not IgG, characteristically neutralizes toxin A in patients with C. difficile diarrhea who develop neutralizing systemic responses. This neutralization of an enteric bacterial toxin is a unique and selective role for serum IgA which provides a novel functional link between the systemic and mucosal immune systems.

Acute Disease↗
PubMed1996

Comparison of PCR-based approaches to molecular epidemiologic analysis of Clostridium difficile.

Representative isolates of the 10 serogroups of Clostridium difficile and 39 clinical isolates (30 toxigenic and 9 nontoxigenic), including 5 isolates from a confirmed nosocomial outbreak, were analyzed by using two previously described arbitrary-primer PCR (AP-PCR) molecular typing methodologies (AP-PG05 and AP-ARB11) and PCR ribotyping. The two AP-PCR methods investigated gave comparable results; AP-PG05 and AP-ARB11 identified 8 and 7 groups among the serogroup isolates and classified the clinical isolates into 21 and 20 distinct groups, respectively. PCR ribotyping also identified 8 unique groups among the serogroup isolates but classified the clinical isolates into 23 groups. In addition, when results obtained by the PCR methods were compared with typing data generated by pulsed-field gel electrophoresis (PFGE), PCR ribotyping and PFGE were found to be in agreement for 83% (29 of 35) of isolates typeable by both techniques while AP-PG05 was in agreement with PFGE for 60% (20 of 33) and AP-ARB11 was in agreement with PFGE for only 44% (17 of 36). These results indicate that PCR ribotyping is a more discriminatory approach than AP-PCR for typing C. difficile and, furthermore, that this technique generates results that are in higher concordance with those obtained by using an established method for differentiating isolates of this organism on a molecular level than are results generated by using AP-PCR.

Bacterial Typing Techniques↗
PubMed2004

Successful treatment with rifampin for fulminant antibiotics-associated colitis in a patient with non-Hodgkin's lymphoma.

A 74-year-old man was admitted to the hospital because of chemotherapy for relapsed non-Hodgkin's lymphoma (NHL). The patient became febrile and experienced diarrhea after chemotherapy. Although ceftazidime and amikacin sulfate were administered as empiric therapy, diarrhea was continued. After several days, stool cytotoxin assay for clostridium difficile (C. difficile) was positive and he was diagnosed as having antibiotics-associated colitis (AAC). Although antibiotics were discontinued and both oral vancomycin and metronidazole were administrated, disease was not improved. To rule out the presence of an additional cause of diarrhea, colon fibroscopic examination was performed. It revealed multiple deep ulcerative lesions at right side colon, surface erosive and minute erosive lesions in all continuous colon. Pseudomembranes were not seen. These findings are compatible with AAC without pseudomembranes. There are no reports that the rifampin is effective on refractory AAC. However, we administered oral rifampin for the current patient. The reasons are 1) conventional antibiotics were not effective, 2) rifampin has excellent in vitro activity against C. difficile, and 3) the efficacy of rifampin on relapsing colitis due to C. difficile is established. After administration of rifampin, fever alleviated and diarrhea was improved. Because AAC may result in significant mortality, patients with refractory or fulminant AAC should be treated with oral rifampin from outset.

Administration, Oral↗
PubMed1996

Prevalence and pathogenicity of Clostridium difficile in hospitalized patients. A French multicenter study.

BACKGROUND: Although Clostridium difficile is the main agent responsible for nosocomial diarrhea in adults, its prevalence in stool cultures sent to hospital microbiology laboratories is not clearly established. OBJECTIVES: To determine the prevalence of C difficile in inpatient stools sent to hospital microbiology laboratories and to assess the relationship between serotypes and toxigenicity of the strains isolated and the clinical data. METHODS: From January 18, 1993, to July 31, 1993, the presence of C difficile was systematically investigated in a case-control study on 3921 stool samples sent for stool culture to 11 French hospital microbiology laboratories. The prevalence of C difficile in this population (cases) was compared with that of a group of 229 random hospital controls matched for age, department, and length of stay (controls). Stool culture from controls was requested by the laboratory although not prescribed by the clinical staff. Serotype and toxigenesis of the strains isolated were compared. RESULTS: The overall prevalence of C difficile in the cases was twice the prevalence in the controls (9.7% vs 4.8%; P < .001) and was approximately 4 times as high in diarrheal stools (ie, soft or liquid) as in normally formed stools from controls (11.5% vs 3.3%; P < .001). The strains isolated from diarrheal stools were more frequently toxigenic than those isolated from normally formed stools. Serogroup D was never toxigenic, and its proportion was statistically greater in the controls than in the cases (45% vs 18%; chi 2 = 5.2; P < .05). Conversely, serogroup C was isolated only from the cases. Clostridium difficile was mainly found in older patients ( > 65 years), suffering from a severe disabling disease, who had been treated with antibiotics and hospitalized for more than 1 week in long-stay wards or in intensive care. CONCLUSIONS: This multicenter period prevalence study clearly supports the hypothesis of a common role of C difficile in infectious diarrhea in hospitalized patients. Disease associated with C difficile should therefore be systematically evaluated in diarrheal stools from inpatients.

Anti-Bacterial Agents↗
PubMed2001

Analysis of expression of GroEL (Hsp60) of Clostridium difficile in response to stress.

Our laboratory has previously shown that adherence of Clostridium difficile to tissue culture cells is augmented by various stresses and that GroEL, a heat shock protein, serves an adhesive function in this bacterium. In this communication, RT-PCR, SDS-PAGE and immunoblotting were used to study the stress response in C. difficile following heat, acid or osmotic shock, iron deprivation or presence of a subinhibitory concentration of ampicillin in the culture medium. All these stresses increased transcription of groEL and production of GroEL to various degrees. Furthermore, the protein was found in membrane fractions and in the extracellular space after heat stress.

Ampicillin↗
PubMed1999

Clostridium difficile colitis associated with infant botulism: near-fatal case analogous to Hirschsprung's enterocolitis.

We present the first five reported cases of Clostridium difficile-associated diarrhea (CDAD) in children with infant botulism caused by Clostridium botulinum. We compare two fulminant cases of colitis in children with colonic stasis, the first caused by infant botulism and the second caused by Hirschsprung's disease. In both children, colitis was accompanied by hypovolemia, hypotension, profuse ascites, pulmonary effusion, restrictive pulmonary disease, and femoral-caval thrombosis. Laboratory findings included pronounced leukocytosis, hypoalbuminemia, hyponatremia, coagulopathy, and, when examined in the child with infant botulism, detection of C. difficile toxin in ascites. CDAD recurred in both children, even though difficile cytotoxin was undetectable in stool after prolonged initial therapy. Four children who had both infant botulism and milder CDAD also are described. Colonic stasis, whether acquired, as in infant botulism, or congenital, as in Hirschsprung's disease, may contribute to the susceptibility to and the severity of CDAD.

Botulism↗
PubMed1994

Comparison of restriction endonuclease analysis, ribotyping, and pulsed-field gel electrophoresis for molecular differentiation of Clostridium difficile strains.

A combined clinical and molecular epidemiologic analysis of 46 strains of Clostridium difficile, including 16 nosocomial isolates from one ward (outbreak ward) plus 17 other nosocomial isolates and 13 community-acquired isolates, was performed. HindIII digests of total cellular DNA were analyzed by restriction enzyme analysis (REA) and ribotyping; SmaI digests were analyzed by pulsed-field gel electrophoresis (PFGE). Isolates were assigned to typing groups on the basis of the profiles detected; isolates with closely related profiles were assigned to subgroups. The 16 isolates from the outbreak ward were resolved by both REA and PFGE into five distinct groups; 13 isolates represented two REA groups and three PFGE groups and two isolates were resolved as distinct groups by both techniques. DNA obtained from one isolate was persistently partially degraded, precluding analysis by PFGE. Seventeen sporadic nosocomial isolates were resolved by REA and PFGE into comparable numbers of groups (i.e., nine groups) and subgroups (i.e., 15 and 14 subgroups, respectively), with two isolates not evaluable by PFGE. The 13 epidemiologically unrelated community-acquired isolates were assigned to 11 groups by REA and to 12 groups by PFGE. Overall, ribotyping identified only nine groups among the 46 isolates. We conclude that REA and PFGE have comparable discriminatory powers for epidemiologic typing of C. difficile isolates and that ribotyping is appreciably less discriminatory. For a few isolates, partial DNA degradation prevented analysis by PFGE but not by REA or ribotyping; the cause of the degradation is unknown.

Bacterial Proteins↗
PubMed2004

A novel method for rapidly diagnosing the causes of diarrhoea.

BACKGROUND: The microbiological diagnosis of infectious diarrhoea may take several days using conventional techniques. In order to determine whether flatus can be used to make a rapid diagnosis, the volatile organic compounds associated with diarrhoea were analysed. METHODS: Stool samples were collected from 35 patients with infectious diarrhoea and from six healthy controls. Gaseous compounds were extracted from a headspace using solid phase microextraction and analysed using gas chromatography and mass spectroscopy. RESULTS: Characteristic patterns of volatile gases were found for the main causes of infectious diarrhoea in hospitals. Furan species without indoles indicated Clostridium difficile, ethyl dodecanoate indicated rotavirus, ammonia without ethyl dodecanoate suggested other enteric viruses, and the absence of hydrocarbons and terpenes indicated Campylobacter infection. CONCLUSION: These results could be the basis of rapid near patient diagnosis of infectious diarrhoea.

Adolescent↗
PubMed1998

Human diseases caused by exotoxins produced by anaerobes and their rapid detection.

Major human diseases caused by exotoxins produced by anaerobes include botulisms, tetanus, foodborne illness caused by enterotoxin-producing Clostridium perfringens, and diarrhea/colitis caused by toxigenic Clostridium difficile. Recently, enterotoxigenic Bacteroides fragilis (ETBF) has been recognized, that may be related to childhood diarrheal disease. Detection test of botulinal neurotoxin is hardly performed at clinical laboratories since the most reliable means of detection and identification of botulinal toxin is by using mouse toxicity and neutralization tests. Clinical laboratories should request the tests to a reference laboratory. Since tetanus is easily diagnosed clinically on the basis of its unique, recognizable sings, the bacteriological tests is not usually requested. C. perfringens foodborne illness can be confirmed by testing stool specimens or the suspect food(s) for enterotoxin by the reversed passive latex agglutination test or counting > 10 5 C. perfringens per g of suspected food or > 10 6 C. perfringens spores per g of stool. Diagnosis of C. difficile-associated diarrhea/colitis is confirmed by detection of toxins A or B of C. difficile and/or recovery of toxigenic C. difficile. Isolation of C. difficile strains or detection C. difficile-speciffic antigen from stool specimens is less diagnostic since nontoxic or toxin A positive-toxin B negative strains are prevalent in Japan. Reliable laboratory tests for ETBF-associated childhood diarrhea are not established yet although ETBF can be proved by polymerase chain reaction for detection of the enterotoxin gene.

Animals↗
PubMed2004

Non-antibiotic associated C. difficile diarrhea in a 7 week-old infant.

We describe a rare case of non-antibiotic associated severe C. difficile diarrhea in a 7-week-old boy. He had massive fluid loss and electrolyte imbalance. He required total parentral nutrition for 10 days and eventually recovered with oral metronidazole. Most of the reported cases in literature are associated with prior antibiotic exposure or in hospitalized patients.

Anti-Infective Agents↗