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PubMed2006

Genotypic and phenotypic analysis of Clostridium difficile correlated with previous antibiotic exposure.

To analyze Clostridium difficile susceptibility results and genotypes in relation to antibiotic exposures that precipitated C. difficile-associated diarrhea (CDAD), we examined 83 nosocomial C. difficile isolates recovered at a tertiary care center in Boston, Massachusetts. MICs were determined by E-test methodology using modified Brucella agar. Isolates were genotyped by pulsed-field gel electrophoresis and restriction enzyme analysis. Antibiotic susceptibilities were: ciprofloxacin (0%), clindamycin (59%), trovafloxacin (63%), ceftriaxone (73%), piperacillin/tazobactam (100%), metronidazole (100%), and vancomycin (100%). The two most common strain groups, isolated from a total of 33 patients, were much more likely to be resistant to clindamycin, erythromycin, and trovafloxacin than other strain groups [79% (26 of 33) versus 2% (1 of 50), respectively]. Clindamycin exposure was strongly associated with CDAD caused by isolates that exhibited multiple resistance to clindamycin, erythromycin, and trovafloxacin (prevalence odds ratio, 4.2; 95% confidence interval, 1.1-16.8), whereas other antimicrobials did not yield significant associations. Resistance of specific C. difficile strains to clindamycin and other antimicrobial agents may contribute to their hospital dissemination and explain, in part, the propensity of clindamycin to trigger nosocomial outbreaks.

Adult↗
PubMed1992

Diarrhea in hospitalized patients.

Clostridium difficle has been associated with diarrhea in hospitalized patients receiving antibiotic therapy and may be nosocomially acquired. Rehabilitation hospital inpatients may require frequent antibiotic intervention and are thus at risk, although few reports of epidemics at such centers have been published. This study describes the impact of C. difficle-related disease among rehabilitation hospital inpatients. A retrospective review was conducted of all inpatients evaluated for diarrhea in two freestanding rehabilitation hospitals over a 13-month period. Clostridium difficle was determined to be the etiologic agent of diarrhea in 36% of the 33 patients, and no other etiologies were identified. Four patients were transferred to acute care because of the severity of symptoms. A total of 120 altered or canceled therapy sessions were observed to occur during the rehabilitative hospital course among studied patients, of which 90% (108) occurred during periods when patients were documented to have been symptomatic for diarrhea. Diarrhea and C. difficile-related disease thus appear to exert an important and adverse impact on the hospital course of these patients, both in terms of medical complications and therapy attendance. Physicians should therefore possess a heightened index of suspicion for C. difficile infection when evaluating patients with diarrhea in this setting. Diagnostic evaluation of rehabilitation hospital inpatients with diarrhea should include C. difficile toxin assay. If the results of the toxin assay are positive, appropriate therapy, including initiation of oral vancomycin or metronidazole and avoidance of antimotility drugs, should be instituted promptly to minimize risk of potential sequelae.

Adult↗
PubMed1998

Chloramphenicol resistance in Clostridium difficile is encoded on Tn4453 transposons that are closely related to Tn4451 from Clostridium perfringens.

The chloramphenicol resistance gene catD from Clostridium difficile was shown to be encoded on the transposons Tn4453a and Tn4453b, which were structurally and functionally related to Tn4451 from Clostridium perfringens. Tn4453a and Tn4453b excised precisely from recombinant plasmids, generating a circular form, as is the case for Tn4451. Evidence that this process is mediated by Tn4453-encoded tnpX genes was obtained from experiments which showed that in trans these genes complemented a Tn4451tnpX delta 1 mutation for excision. Nucleotide sequencing showed that the joint of the circular form generated by the excision of Tn4453a and Tn4453b was similar to that from Tn4451. These results suggest that the Tn4453-encoded TnpX proteins bind to similar DNA target sequences and function in a manner comparable to that of TnpX from Tn4453. Furthermore, it has been shown that Tn4453a and Tn4453b can be transferred to suitable recipient cells by RP4 and therefore are mobilizable transposons. It is concluded that, like Tn4451, they must encode a functional tnpZ gene and a target oriT or RSA site. The finding that related transposable elements are present in C. difficile and C. perfringens has implications for the evolution and dissemination of antibiotic resistance genes and the mobile elements on which they are found within the clostridia.

Base Sequence↗
PubMed2000

Isolation of environmental Clostridium difficile from a veterinary teaching hospital.

An environmental survey of a veterinary teaching hospital for the presence of Clostridium difficile was performed using contact plates and cycloserine-cefoxitin-fructose with 0.1% sodium taurocholate agar. Clostridium difficile was isolated from 24 of 381 sites (6.3%). Growth was obtained from 4.5% (9/202) of sites sampled in the Large Animal Clinic, from 8.1% (13/160) of sites within the Small Animal Clinic, and from 20% (2/10) of sites sampled elsewhere. Fourteen of 21 strains tested produced toxins in vitro. A geographic association was found with areas in the large animal clinic where nosocomial C. difficile diarrhea in horses had previously been diagnosed. Several other sites with a potential for nosocomial transmission of the organism were identified. Areas from which C. difficile was isolated tended to be areas with high animal traffic, with increased chance of fecal contamination, and with rough, difficult to clean surfaces. This study documents the prevalence of this organism in the environment and its potential role in nosocomial disease.

Animals↗
PubMed2006

Antibiotic-associated diarrhoea.

Diarrhoea is a common complication of antimicrobial therapy. The term antibiotic-associated diarrhoea (AAD) is often considered synonymous with Clostridium difficile. In fact, AAD can develop through a variety of mechanisms and manifest through a broad range of clinical signs and symptoms. For improved prevention and recognition of AAD, it is important to understand the pathophysiology and risk factors for AAD. Although Clostridium difficile continues to be the most common identifiable pathogen of AAD, many patients with AAD can be managed through a variety of conservative measures. This review focuses on some of the important distinctions between nonspecific AAD and antibiotic-associated colitis. In addition, the most recent data on important risk factors for the development of AAD are summarised. Given its pathogenicity, there will be an emphasis on the early diagnosis, treatment and prevention of Clostridium difficile-associated diarrhoea. AAD is a common clinical problem that can progress to severe, life-threatening disease if not recognised quickly. Better awareness of risk factors can lead to the most efficacious treatment of this disorder: primary prevention.

Anti-Bacterial Agents↗
PubMed2002

[PCR cloning of 3'-terminal repeat fragments of Clostridium difficile toxin A and toxin B gene].

OBJECTIVE: To explore a method to rapidly detect the presence of Clostridium difficile. METHODS: PCR was used to amplify DNA fragments from the highly conserved and repeated domains of the 3'-terminal of Clostridium difficile toxin A gene and toxin B genes. RESULTS: The fragments 960 bp and 1,851 bp in length were respectively amplified from toxin A and toxin B, while the control bacteria presented no distinct results. CONCLUSION: The 960 bp and 1,851 bp fragments are specific for Clostridium difficile and PCR can be used to detect Clostridium difficile from the stool. As the peptides encoded by these conserved domains have high hydrophobicity and strong antigenicity, manufacture of the protein vaccine by gene engineering is possible on the basis of these conserved domains.

Bacterial Proteins↗
PubMed1995

Detection of Clostridium difficile toxins from the small intestine and cecum of rabbits with naturally acquired enterotoxemia.

Four specific-pathogen-free rabbits with anorexia died peracutely; decreased fecal output, nasal exudate, and labored breathing were the only other clinical abnormalities observed in two of the rabbits before death. The animals, three juveniles and one adult, were on a standard polyclonal antibody production regimen and had received immunizations approximately 2 weeks before presentation. External examination revealed distended abdomen and perineal fecal staining. At necropsy the small intestine was distended with fluid, and the cecum was distended with chyme. The small intestines and cecum had marked serosal hyperemia. Anaerobic bacterial culture techniques were used to isolate Clostridium difficile from the small intestine (3/4) and cecum (2/4). In all cases C. difficile toxin B was detected at high titers (10(2) to > 10(5)) in the small intestine by cytotoxicity assay with HeLa 229 cell culture. In two of the four rabbits C. difficile was isolated, and cytotoxin titers were detected at 10(1) and 10(4) in the cecum of affected rabbits. Toxin B was neutralized with C. sordellii antiserum but not C. spiroforme antiserum. In addition, toxin A was detected in each of the cytotoxin B-positive samples by a commercial toxin A enzyme immunosorbent assay. In vitro production of toxins A and B was detected from each culture isolate after incubation in chopped meat broth. These cases are noteworthy because spontaneous (nonantibiotic-associated) C. difficile enterotoxemia has not been previously reported in rabbits. Also the toxins of clostridial organisms are usually documented in the cecum, not the small intestine, of rabbits.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

[Pseudomembranous colitis after surgery for a ruptured abdominal aortic aneurysm].

We present a rare postoperative complication after surgical procedures for rupture of abdominal aortic aneurysms. The disease, a pseudomembranous colitis, was early recognized (by evidence of clostridium difficile after a coprocultive) and satisfactorily treated with vancomycin. From the literature review we found only a similar case but results were absolutely different from our case.

Aged↗
PubMed1995

Effects of purified Clostridium difficile toxin A on rabbit distal colon.

BACKGROUND & AIMS: Antibiotic-associated pseudomembranous colitis in humans is caused by proliferation of Clostridium difficile, which elaborates an enterotoxin toxin A that causes epithelial damage and altered motility in rabbit small intestine. The aim of this study was to assess the effects of toxin A on rabbit distal colonic motility and to relate this to histological damage and inflammatory mediator production. METHODS: Two hundred micrograms per milliliter of toxin A was placed in a distal colonic loop in anesthetized rabbits, and myoelectric activity was recorded for the following 7 hours. The colon was histologically evaluated and assayed for eicosanoid production. The effects of toxin A on longitudinal and circular muscle were also assessed in vitro. RESULTS: Beginning 1 hour after instillation, toxin A caused a significant increase in the number of spike bursts without altering slow wave frequency; this was associated with an increase in mucosal neutrophils and increased production of prostaglandin E2 and leukotrienes B4 and C4/D4/E4. Seven hours after administration of toxin A, mediator levels and myoelectric activity remained increased but significant mucosal damage was now also present. Toxin A did not affect longitudinal or circular muscle in vitro. CONCLUSIONS: C. difficile toxin A caused a significant neutrophil infiltration and an increased myoelectric activity before producing mucosal damage. The myoelectric effect may be indirect, resulting from the production of motility-altering arachidonic acid metabolites.

Animals↗
PubMed2006

Antimicrobial resistance of Clostridium difficile isolates in a tertiary medical center, Israel.

The antimicrobial susceptibilities of 49 Clostridium difficile isolates obtained from patients with C. difficile-associated diarrhea to metronidazole, vancomycin, rifampicin, fusidic acid, doxycycline, and linezolid were determined by the disc diffusion and Etest (Biodisk, Solna, Sweden). Random amplification of polymorphic DNA-PCR amplification assay was performed for studying clonality of isolates. Resistance to metronidazole was found in 2% (1/49 isolates; MIC > or = 256 microg/mL) of isolates and resistance to linezolid in 2% (1/49 isolates; MIC = 24 microg/mL). One isolate showed combined resistance to fusidic acid (by disc diffusion test) and rifampicin (MIC > or = 32 microg/mL). All isolates were sensitive to doxycycline and vancomycin. Molecular typing revealed an absence of clonality among the resistant isolates, whereas the sensitive isolates were monoclonal. Resistance of C. difficile to metronidazole and other antimicrobials including linezolid exists in our institution. This finding should promote exploration of this problem in Israel and clarify the impact of resistance on outcome.

Adolescent↗
PubMed2006

Epidemiology and incidence of Clostridium difficile-associated diarrhoea diagnosed upon admission to a university hospital.

Patients with Clostridium difficile-associated diarrhoea (CDAD) may initially develop symptoms in the community and be subsequently diagnosed at hospital admission. At the present time there is no national surveillance system and no standardized case definition of CDAD in the USA, and baseline data on the incidence and epidemiology of CDAD are scarce. The objective of this study was to report the incidence of CDAD at a tertiary care hospital, and to determine the epidemiology of cases diagnosed within 48h of hospital admission, compared with cases of nosocomial CDAD diagnosed 48h or more after hospitalization. The average incidence was 4.0 cases/10 000 patient-days for CDAD on admission and 7.0 cases/10 000 patient-days for nosocomial CDAD. A significant difference was observed in CDAD rates on admission compared with nosocomial CDAD rates (P=0.017), but no differences were observed over time for either rate. Overall, 44% of cases had CDAD on admission and 56% of cases had nosocomial CDAD. Fifty-six (62%) patients with CDAD on admission had been admitted to the same hospital and 24 (27%) had been admitted to another hospital within the previous 90 days. Only eight (9%) patients had not been exposed to any healthcare services in the 90 days preceding hospital admission. A standardized case definition of healthcare-associated CDAD should include previous hospitalizations. Admitting physicians should consider C. difficile in the differential diagnosis of patients admitted with diarrhoea, with or without a history of admission to healthcare facilities.

Adult↗
PubMed1994

Identification of outbreak-associated and other strains of Clostridium difficile by numerical analysis of SDS-PAGE protein patterns.

Seventy-three cultures of Clostridium difficile isolated both during, and in the period immediately following, an outbreak of infection in a group of three hospitals, were characterized by one-dimensional sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) of whole-cell proteins. Each protein pattern was characterized by the presence of one or two dense bands which were highly reproducible. The protein patterns were used as the basis for a numerical analysis which divided the strains into five phenons (electrophoretic or EP types). The majority, 60 of the 73 cultures, belonged to a single phenon which included strains from both patients and the environment. We conclude that high-resolution SDS-PAGE of proteins provides an effective method for typing C. difficile and therefore for tracing the possible spread of epidemic strains in hospitals and other institutions, thereby allowing a better understanding of the epidemiology of the organism.

Adult↗
PubMed1998

Determination and validation of a predictive model for Clostridium difficile diarrhea in hospitalized oncology patients.

BACKGROUND: Clostridium difficile colitis in the cancer patient receiving chemotherapy is a frequent cause of morbidity which may prolong hospitalization. Techniques for identifying infection often delay the initiation of therapy. PATIENTS AND METHODS: In this retrospective case-control analysis, we identified predictors for C. difficile-associated diarrhea in 29 patients hospitalized from 1988 to 1993 on a hematologic malignancy/bone marrow transplant unit (hospital A). We then validated our model with 58 C. difficile cases and 74 controls admitted to an oncology unit from a different institution (hospital B). RESULTS: We found that low intensity of chemotherapy (P < 0.001), lack of parenteral vancomycin use (P = 0.03) and hospitalization within the past two months (P = 0.05) were independently predictive of C. difficile colitis by multivariate analysis. These variables were weighted for predictive capability using a receiver operator characteristic score; low intensity chemotherapy was assigned two points, lack of parenteral vancomycin received one point and prior hospitalization one point (P < 0.001 by chi 2 for trend). The receiver operating characteristic (ROC) curve areas were 0.78 for patients at hospital A and 0.70 at hospital B indicating moderate drop off in discrimination. Compared to hospital A patients, hospital B patients hospitalized between 1989 and 1994 were more often women (P = 0.04), received less systemic vancomycin (P = 0.01), were less frequently neutropenic (P < 0.05), and received less intense chemotherapy regimens (P < 0.05). Despite these differences in demographics in patients between these institutions, our predictive model was validated in hospital B patients (P = 0.02 by chi 2 for trend). CONCLUSIONS: The results of this study may help clinicians predict the risk of C. difficile disease in the hospitalized immunocompromised oncology patient and may help guide empiric therapy while awaiting results of stool toxin assays.

Case-Control Studies↗
PubMed2004

"Collateral damage" from cephalosporin or quinolone antibiotic therapy.

"Collateral damage" is a term used to refer to ecological adverse effects of antibiotic therapy; namely, the selection of drug-resistant organisms and the unwanted development of colonization or infection with multidrug-resistant organisms. The risk of such damage can be assessed for different antibiotic classes by a variety of epidemiologic studies. Cephalosporin use has been linked to subsequent infection with vancomycin-resistant enterococci, extended-spectrum beta-lactamase-producing Klebsiella pneumoniae, beta-lactam-resistant Acinetobacter species, and Clostridium difficile. Quinolone use has been linked to infection with methicillin-resistant Staphylococcus aureus and with increasing quinolone resistance in gram-negative bacilli, such as Pseudomonas aeruginosa. Neither third-generation cephalosporins nor quinolones appear suitable for sustained use in hospitals as "workhorse" antibiotic therapy.

Anti-Bacterial Agents↗
PubMed1995

Transient expression of RhoA, -B, and -C GTPases in HeLa cells potentiates resistance to Clostridium difficile toxins A and B but not to Clostridium sordellii lethal toxin.

The bacterial pathogen Clostridium difficle synthesizes two high-molecular-weight toxins (A and B), which exhibit toxic effects in vivo and in vitro. Here, we present evidence that the major intracellular targets of these two toxins are the Rho GTPases. Overexpression of RhoA, RhoB, or RhoC GTPases in transfected HeLa cells conferred an increased resistance to toxins A and B, indicating that these toxins cause their cytopathic effects primarily by affecting Rho proteins. In addition, toxin A and B treatment appeared to result in modification of Rho, since Rho isolated from toxin-treated cells had a decreased ability to be ADP-ribosylated by Clostridium botulinum C3 exoenzyme. In contrast, the lethal toxin (LT) of Clostridium sordellii, although structurally and immunologically related to C. difficile toxin B, appeared to induce cytopathic effects independently of the Rho GTPases. Overexpression of RhoA in transfected HeLa cells did not protect them from the effect of LT, and Rho isolated from lysates of LT-treated cells was not resistant to modification by C3. Immunofluorescence studies showed that LT treatment caused a cytopathic effect that was very different from those described for C. difficile toxins A and B, resulting in an increase in cortical F-actin, with a concomitant decrease in the number of stress fibers, and in the formation of numerous microvilli containing the actin-bundling protein fimbrin/plastin.

Bacterial Proteins↗
PubMed1999

Evaluation of different methods for detection of Clostridium difficile toxins in Poland.

The aim of this study was to compare different methods for C. difficile toxins detection. Fifty three stool samples taken from patients with antibiotic-associated diarrhoea were studied. TCD toxin A EIA (Becton Dickinson, USA), Tox A/B ELISA test (TechLab, USA), cytotoxicity and neutralization assay on McCoy cells and PCR for detection of both toxin A and B genes were performed in vivo (in stool samples) and in vitro (in isolated strains). Reference toxigenic and nontoxigenic and two Japanese toxin A-negative and toxin B-positive C. difficile strains were used as a controls. TCD toxin A EIA detected in vivo only 19 positive samples. Tox A/B test detected 52 positive samples out of 53 studied. All 53 stool samples were C. difficile culture positive (53 strains were cultured). Toxin B was detected in 52 strain-supernatants and in all controls (except the nontoxigenic one). Both toxin A and B genes were detected by PCR in all 53 isolated strains, Japanese and reference strain (except the nontoxigenic one). In vitro toxin A was detected by TCD toxin A EIA in 42 strains. These results were compared with those obtained in Tox A/B ELISA test. We observed 52 positive strains. Toxigenic reference strain and two Japanese toxA(-)/toxB(+) strains were also positive. Only 2 negative results were obtained with the nontoxigenic reference strain and unique nontoxigenic isolated strain. Tox A/B ELISA test seems to be the best for detection of C. difficile toxins in vivo and in vitro. Test avoids the false-negative results in the case of presence of toxin A-negative and toxin B-positive strain.

Anti-Bacterial Agents↗