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PubMed2003

New types of toxin A-negative, toxin B-positive strains among Clostridium difficile isolates from Asia.

A total of 56 C. difficile strains were selected from 310 isolates obtained from different hospitals in Japan and Korea and from healthy infants from Indonesia. Strains that had been previously typed by pulsed-field gel electrophoresis and PCR ribotyping, were characterized by toxinotyping and binary toxin gene detection. When toxinotyped, 35 strains were determined to be toxinotype 0, whereas 21 strains showed variations in toxin genes and could be grouped into 11 variant toxinotypes. Six of the toxinotypes had been described before (I, III, IV, VIII, IX, and XII). In addition, five new toxinotypes were defined (XVI to XX). Three of the new toxinotypes (XVIII, XIX, and XX) vary only in repetitive regions of tcdA and produce both toxins. In two strains from toxinotypes XVI and XVII, the production of TcdA could not be detected with commercial immunological kits. Strain J9965 (toxinotype XVII) was in PaLoc similar but not identical to another known A(-)B(+) strain, C. difficile 8864. Strain SUC 36 (toxinotype XVI), on the other hand, was similar to well-defined group consisting of toxinotypes V, VI, and VII, which thus far includes only A(+)B(+) strains. Toxinotypes XVI and XVII represent two new groups of A(-)B(+) strains. Strains of the well-known A(-)B(+) group from toxinotype VIII have a nonsense mutation at the beginning of tcdA gene, and the introduction of a stop codon at amino acid position 47 results in nonproduction of TcdA. The 5'-end sequence of tcdA in two newly described A(-)B(+) strains does not contain an identical mutation. The prevalence of variant C. difficile strains varied greatly among nine hospitals. Only five strains from four different hospitals were positive in PCR for amplification of the binary toxin gene.

Amino Acid Sequence↗
PubMed1992

Selective criteria for the microbiological examination of faecal specimens.

To assess the effectiveness of predetermined investigation criteria for the examination of faecal samples from inpatients, cultured stool specimens were prospectively examined for Salmonella spp, Shigella spp, Campylobacter spp and Clostridium difficile, and screened microscopically for intestinal parasites. Out of a total of 505 specimens, 421 (83%) fulfilled the criteria for examination for C difficile, 254 (50%) for Salmonella spp, Shigella spp, and Campylobacter spp, and 87 (17%) for intestinal parasites. Isolation rates for these organisms in those groups of patients where examination was indicated were 22.5% for C difficile and 9.1% for Salmonella spp, Shigella spp, and Campylobacter spp; the detection rate for parasites was 3.5%. In those patients where the criteria did not suggest investigation, the isolation or detection rates were 3.6% for C difficile, 0% for Salmonella spp, Shigella spp, and Campylobacter spp, and 1.7% for intestinal parasites, suggesting that the use of predetermined investigation criteria was effective.

Animals↗
PubMed2005

Clostridium difficile causing acute renal failure: case presentation and review.

AIM: Clostridium difficile infection is primarily a nosocomial infection but asymptomatic carriers of Clostridium difficile can be found in up to 5% of the general population. Ampicillin, cephalosporins and clindamycin are the antibiotics that are most frequently associated with Clostridium difficile-associated diarrhea or colitis. Little is known about acute renal failure as a consequence of Clostridium difficile-associated diarrhea. METHODS: In this case report, we describe the course of Clostridium difficile-associated diarrhea in an 82-year-old patient developing acute renal failure. Stopping the offending agent and symptomatic therapy brought a rapid improvement of diarrhea and acute renal failure, full recovery was gained 18 d after admission. In a systematic review we looked for links between the two conditions. RESULTS: The link between Clostridium difficile-associated diarrhea and acute renal failure in our patient was most likely volume depletion. However, in experimental studies a direct influence of Clostridium difficile toxins on renal duct cells could be shown. CONCLUSION: Rapid diagnosis, nonspecific supportive treatment and specific antibiotic treatment, especially in the elderly, may lower excess mortality Clostridium difficile-associated diarrhea and renal failure being possible complications.

Acute Kidney Injury↗
PubMed2002

[Clostridium difficile strains not producing Toxin A, but producing Toxin B [toxA(-)tox B(+)]--etiologic agent of antibiotic associated diarrhoea (AAD) in Poland].

Previously, toxin A-negative/toxin B-positive Clostridium difficile strains were not thought to be associated with clinically significant diseases. In our study among 159 tested C. difficile strains isolated from feacal samples from 413 patients with antibiotic associated diarrhoea (AAD) 17 strains (11%) were negative in the "Culturette Brand Toxin" CD (Becton-Dickinson) for detection toxin A and positive in the TOX A/B test, designed for detection of both toxins. The conserved regions of both toxin genes were detectable in all of isolates studied by the PCR. Nine of these C. difficile strains had a deletion in the A gene and remaining 8 strains, revealed an amplicon with the expected size of approximately 2500 bp. In this paper we described the first time the toxin A-negative/toxin B-positive C. difficile strains with deletion in toxin A gene, isolated from the faecal samples of patient with AAD in Poland.

Anti-Bacterial Agents↗
PubMed1992

[Clostridium difficile and diarrhea in infants in the first half-year of life].

In order to study a possible etiological relationship between Clostridium and diarrhea in children of the first half year of life and to characterize the colonization of the intestine with these bacteria, bacteriological investigations of feces were carried out in neonates and babies aged 1, 4 and 14 days and 1, 3 and 6 months. The development of the children and their health status were monitored under home conditions. It has been established that the colonization of the neonates' intestine with Clostridium including C. Difficile occurs within the early times (since the 4th day of life). Later the colonization with C. difficile becomes wavy in nature. Among 7 types of Clostridium isolated from the intestine of the children, C. difficile occurred most frequently (29.1%). The overwhelming majority of the strains of these bacteria produced toxin whose activity did no exceed 10(-1)-10(-2). The cytopathic effect was mostly demonstrable in 72 hours. No convincing evidence was obtained about the etiological importance of C. difficile in the development of diarrhea in the children placed under observation. It is likely that the latter one was due to the disturbance of intestinal biocenosis, that manifested by profound quantitative disorders (proliferation of the opportunistic aerobic flora, a dramatic reduction of the content of bifido- and lactic acid bacteria up to their complete absence). At the same time a great number of children carrying C. difficile attests to a potential development of specific diarrheas (under hospital conditions and during massive antibacterial therapy).

Bacteriological Techniques↗
PubMed1992

Cytotoxicity of Clostridium difficile toxin A for human colonic and pancreatic carcinoma cell lines.

The use of bacterial exotoxins may constitute novel adjuncts to treatment of gastrointestinal tract malignancies. Clostridium difficile toxin A was evaluated for its cytotoxic effect in vitro on 24 human cell lines and strains including carcinomas of the colon, pancreas, prostate, lung, breast, and lymphoid malignancies, as well as nonmalignant tissues. All nine colon and five pancreas cell lines were extraordinarily sensitive to the cytotoxic effect of Clostridium difficile toxin A at very low concentrations. This effect, which occurred rapidly and was dose dependent, was observed in all cells of seven colon and two pancreas cell lines at concentrations as low as 1-5 ng/ml (10(-12) to 10(-11) M), whereas cells derived from other sites required 60 to greater than 500 ng/ml to achieve an equivalent effect. The data suggest that Clostridium difficile toxin A may have potential therapeutic value in the treatment of some gastrointestinal tract cancers.

Bacterial Toxins↗
PubMed2005

Eradication of enteric helicobacters in Mongolian gerbils is complicated by the occurrence of Clostridium difficile enterotoxemia.

Outbred Mongolian gerbils from a United States commercial source were examined for colonization with naturally occurring enterohepatic Helicobacter spp. Helicobacter spp. were identified in the cecum and colon by culture and by using genus-specific primers in polymerase chain reaction (PCR) assays. Nutritionally balanced triple-antibiotic wafers (containing amoxicillin, metronidazole, and bismuth) used previously to eliminate helicobacter infections in mice were administered in an attempt to eradicate the naturally occurring novel helicobacters in the gerbils. After 7 days of antibiotic treatment, two of the experimental animals died due to Clostridium difficile-associated enterotoxemia. However, at 3 weeks after antibiotic cessation, the surviving three animals had no Helicobacter spp. in the cecum or colon according to PCR analysis. Eradication of Helicobacter spp. using dietary administration of antibiotics was complicated by the presence of toxin-producing C. difficile. An alternate method to develop helicobacter-free gerbils (such as Caesarian rederivation) may be necessary.

Animals↗
PubMed1998

Protease activity of Clostridium difficile strains.

The production of proteolytic enzymes by 10 Clostridium difficile isolates of varying toxigenicity and clinical origin was studied to determine if all isolates secreted proteases. Different protease substrates were studied: gelatin, collagen, phenylazobenzyloxycarbonyl-leucyl-glycyl-L-prolyl-D-arginine (Pz-peptide), casein, azocasein, and azocoll. All isolates degraded gelatin, collagen, and azocoll. The supernatants of all isolates contained an enzyme capable of attacking gelatin incorporated in a polyacrylamide gel (zymograms) and forming two closely spaced lytic bands with an estimated molecular mass of 35-40 kDa. Polyclonal antibodies, produced against the C. difficile gelatinase, revealed in Western blots a 35-kDa protein in the culture supernatants of all C. difficile isolates. In the same manner, Clostridium perfringens collagenase polyclonal antibodies detected a 120-kDa protein in the culture supernatants of all isolates; this suggests that at least two proteases may exist in C. difficile. The protease activities of the 10 strains examined did not seem strikingly different quantitatively but were in general weak and their role in pathogenicity is suspect.

Caseins↗
PubMed2006

Ileal perforation secondary to Clostridium difficile enteritis: report of 2 cases.

Two cases of small-bowel perforation secondary to Clostridium difficile enteritis are described and compared with the 8 cases of C difficile enteritis reported in the medical literature. The cause of small-bowel involvement with C difficile is unknown, but prior antibiotic use, prior colectomy, chronic alterations in small-bowel flora, and other host factors are discussed.

Aged, 80 and over↗
PubMed1999

Laboratory diagnosis of toxigenic Clostridium difficile by polymerase chain reaction: presence of toxin genes and their stable expression in toxigenic isolates from Japanese individuals.

Clostridium difficile causes pseudomembranous colitis and antibiotic-associated diarrhea. The definitive diagnosis of C. difficile infection is finally accomplished by the isolation of toxigenic C. difficile. However, only a small number of Japanese clinical laboratories are able to reach a definitive diagnosis of C. difficile infection, probably because simple reliable assays for toxins in the isolates are not available. In this study, we examined the compatibility of a polymerase chain reaction (PCR) assay and tissue culture assay to identify toxigenic C. difficile, in toxigenic and nontoxigenic C. difficile isolates from Japanese patients and healthy carriers. The specificity of PCR primers was demonstrated by restriction endonuclease digestion and seminested PCR in C. difficile VPI 10463 strain. No PCR product was amplified in the eight other clostridial species used to check the specificity of the PCR assay. The detection limit was 10(3) cells. Both toxin A and toxin B genes (the genes encoding the major virulence factors of C. difficile) were detected in 58 toxigenic C. difficile isolates, which showed a wide range of cytotoxic activity in tissue culture assays. Neither of the toxin genes was carried by 40 nontoxigenic strains of C. difficile. The results of this study strongly suggest that a definitive diagnosis of C. difficile infection can be accomplished by PCR detection of the toxin genes rather than by tissue culture assay of isolates.

Adult↗
PubMed2001

Nosocomial outbreak of Clostridium difficile-associated diarrhoea due to a clindamycin-resistant enterotoxin A-negative strain.

A clindamycin-resistant toxin A-negative, toxin B-positive Clostridium difficile strain caused an outbreak among 24 hospitalized patients at the Department of Surgery, the Intensive Care unit, and the Department of Internal Medicine of an 800-bed academic hospital. Nineteen patients had undergone a surgical intervention and all 24 patients received at least one dose of antibiotics prior to the development of Clostridium difficile-associated diarrhoea. Twenty-seven episodes of Clostridium difficile-associated diarrhoea in 24 patients were categorized as mild (n=19), severe (n=7), or fatal (n=1). Relapses occurred in three patients. Nineteen of the 27 episodes required anti-Clostridium difficile treatment. Molecular typing performed by arbitrary primer polymerase chain reaction (PCR) and PCR amplification of rRNA intergenic spacer regions revealed that the outbreak strains recovered from culture were identical. The outbreak strain belonged to serogroup F and was resistant to erythromycin, clindamycin, and tetracycline, whereas susceptibility to chloramphenicol varied. No phenotypic activity of enterotoxin A was detected. A deletion of approximately 1.7 kb was found in the toxin A gene. Cytotoxin B had an unusual effect on cell culture assays that, at first, was not recognized as Clostridium difficile specific but could be neutralized with anti-Clostridium difficile B cytotoxin.

Adult↗
PubMed1998

Effect of isoleucine on toxin production by Clostridium difficile in a defined medium.

Supplementation of a carbohydrate-free minimal medium with a high level (100 mM) of histidine, methionine, valine, isoleucine, proline and leucine, in particular isoleucine, markedly increased toxin production by Clostridium difficile VPI 10463. The effect of isoleucine was further examined. Increasing the concentration of isoleucine from 20 to 100 mM remarkably increased toxin production, while bacterial growth decreased gradually. Amino acid analysis of the culture revealed that, at 100 mM isoleucine, consumption of isoleucine was remarkably increased. During the incubation period when toxin titers increased markedly but bacterial growth was declining, isoleucine, leucine and cysteine were taken up preferentially and alanine and cystathionine, which were not found at 1 mM isoleucine, were produced in large quantities. These findings suggest that isoleucine may play an important role in toxin production by C. difficile and that alanine and cystathionine production may be co-regulated with the toxin production in the absence of fermentable carbohydrates.

Amino Acids↗
PubMed2001

Liver abscess caused by Clostridium difficile.

We report the first case of an infected cyst and liver abscess caused by Clostridium difficile. It recurred 11 months later, despite therapy with vancomycin and percutaneous drainage. Administration of metronidazole following percutaneous drainage achieved a favorable outcome.

Aged↗
PubMed2002

Conditions associated with leukocytosis in a tertiary care hospital, with particular attention to the role of infection caused by clostridium difficile.

Few modern studies have enumerated the conditions associated with leukocytosis. Our clinical experience has implicated Clostridium difficile infection in a substantial proportion of patients with leukocytosis. In a prospective, observational study of 400 inpatients with WBC counts of >/=15,000 cells/mm(3), we documented >/=1 infection in 207 patients (53%). Of these 207 patients, 97 (47%) had pneumonia, 60 (29%) had urinary tract infection, 34 (16%) had soft-tissue infection, and 34 (16%) had C. difficile infection. C. difficile infection was present in 25% of patients with WBC counts of >30,000 cells/mm(3) who did not have hematological malignancy. Other causes of leukocytosis in the 400 patients included physiological stress, in 152 patients (38%); medications or drugs, in 42 (11%); hematological disease, in 22 (6%); and necrosis or inflammation, in 22 (6%). C. difficile infection is a prominent cause of leukocytosis and this diagnosis should be considered for patients with WBC counts of >/=15,000 cells/mm(3), even in the absence of diarrheal symptoms.

Adult↗
PubMed2003

Prevention of fatal Clostridium difficile-associated disease during continuous administration of clindamycin in hamsters.

Clostridium difficile-associated disease (CDAD) due to toxigenic strains is prevented in hamsters by colonization by nontoxigenic C. difficile after administration of clindamycin (Cm). To prevent CDAD during treatment with antibiotics, we gave a Cm-resistant nontoxigenic C. difficile strain, M13 (minimal inhibitory concentration [MIC], >256 microg/mL), and a Cm-susceptible strain, M3 (MIC, 0.5 microg/mL), to hamsters receiving Cm daily for days 1-5. Either M13 or M3 was given orogastrically (1 x 10(6) spores/day) to each hamster in 3 groups of 5 each, on either day 3, days 3-5, or days 3-7. M13 colonized at a higher rate and faster than did M3 (P<.001). When hamsters were challenged by toxigenic strain B1 on days 5, 7, or 9, M13 prevented CDAD in 100% of the hamsters. M3 protected no hamsters challenged by B1 on day 5, 20% on day 7, and 100% on day 9. M13 contains the erm(B) resistance gene but not the mobilizable element Tn5398. The benefits of use of Cm-resistant nontoxigenic C. difficile to prevent CDAD must be balanced against the risk that resistance might be transferred to other enteric bacteria.

Adhesins, Bacterial↗
PubMed1997

Successful control of Clostridium difficile infection in an elderly care unit through use of a restrictive antibiotic policy.

Toxin-producing Clostridium difficile is the commonest bacterial cause of nosocomial diarrhoea and is a well recognized cause of hospital outbreaks in elderly care units. High C. difficile disease rates have been associated with the use of broad-spectrum antibiotics, especially cephalosporins. An outbreak of C. difficile infection in the elderly care unit at Gloucestershire Royal NHS Trust continued despite increased ward cleaning and strict implementation of infection control measures. A restrictive antibiotic policy that would maintain colonization resistance in the gastrointestinal tract was introduced throughout this unit. Patients admitted with suspected infection were prescribed intravenous (i.v.) benzylpenicillin 1.2-1.8 g every 6 h to cover streptococcal infections and i.v. trimethoprim 200 mg twice daily to cover urinary tract pathogens and Haemophilus influenzae. If the patient had septic shock a single iv dose of gentamicin was given (120-180 mg) to cover more resistant gram-negative bacilli. The following were monitored before and after the policy change. The number of cases of C. difficile toxin-positive diarrhoea; cefuroxime and total antibiotic use on the elderly care wards; patient mortality rates; and length of hospital stay: two hundred and fifty-two and 234 patients respectively with a discharge diagnosis of infection were admitted before and after the antibiotic policy change. Mortality rates and length of hospital stay were unchanged. Cefuroxime prescribing and total antibiotic prescribing costs fell by 5150 pounds sterling and 8622 pounds sterling respectively in the 7 month period after the change. Thirty-seven cases of C. difficile diarrhoea occurred in the period before and 16 in the period after the policy change. The incidence of C. difficile diarrhoea and of cefuroxime use has remained low since then. The use of narrow-spectrum antibiotics for hospital treatment of community-acquired infections in the elderly should be encouraged. Outbreaks of C. difficile diarrhoea should be managed with the combined approach of infection control and strict antibiotic policies.

Aged↗
PubMed1993

Demonstration of toxin A and B by polymerase chain reaction and McCoy cell assay in clinical isolates of Clostridium difficile from Denmark.

A polymerase chain reaction (PCR) for demonstration of gene fragments of Clostridium difficile was established. One hundred and sixty-eight clinical isolates of C. difficile from three population groups were tested for production of cytotoxins by McCoy cell line assay (MCA) and for fragments of toxin A and B genes by PCR. The fragments for PCR amplification were at the 5' end of the toxin genes, which was found to be specific for C. difficile. Full agreement between the PCR and MCA results was found with respect to toxicity. Fifty-eight of the 168 strains were cytotoxin positive. Isolates from 41 normal healthy children did not differ regarding cytotoxicity compared to isolates from hospitalized children. In adult hospitalized patients a much higher frequency of toxin-producing isolates was found. In two strains from two children, not of the same family, only the toxin A gene fragment was demonstrated, indicating that some strains of C. difficile only harbour the gene for enterotoxin. When two isolates from different periods of time were tested from 36 of the healthy children, a variation in cytotoxicity was found: in seven children strains changed from non-toxic to toxic and in four vice versa. This may be explained by a fluctuating colonization of toxic and non-toxic C. difficile strains, or it may indicate the need for examination of more than one strain from a positive faecal sample to demonstrate cytotoxicity.

Adult↗