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PubMed2006

Vancomycin-induced elevation of liver enzyme levels.

OBJECTIVE: To report a case of oral vancomycin-induced elevation of liver enzyme levels. CASE SUMMARY: A 57-year-old man with multiple medical conditions requiring systemic antibiotic therapy developed numerous Clostridium difficile-associated enterocolitis episodes. The patient did not respond adequately to oral metronidazole, as evidenced by his continuing diarrhea. He was treated with oral vancomycin on 5 separate occasions (with doses from 125 to 500 mg/day), each of which resulted in significant elevations in alanine aminotransferase (to 371 U/L) and aspartate aminotransferase (to 203 U/L) levels. The elevations resolved on each occasion with discontinuation of vancomycin. DISCUSSION: Vancomycin, a glycopeptide antibiotic, has primary activity against gram-positive bacteria. Oral vancomycin can be used for the treatment of C. difficile-associated enterocolitis in patients who fail to respond to or are intolerant to metronidazole therapy. Oral vancomycin has very poor bioavailability and, as of May 4, 2006, has not been associated with hepatic toxicity. Inflammatory bowel disease processes can result in increased absorption of oral vancomycin. CONCLUSIONS: This is the first reported case of oral vancomycin-induced elevation of hepatic enzyme levels. Use of the Naranjo probability scale indicated that this was a probable adverse drug-associated event.

Alanine Transaminase↗
PubMed2003

[Detection of ermB gene responsible for high level resistance to clindamycin (MLS type resistance) among Clostridium difficile strains isolated from antibiotic associated diarrhea (AAD)].

In 68 C. difficile strains isolated from feacal samples of patients with antibiotic associated diarrhoea (AAD) investigated presence of ermB gene transferable of high level resistance to clindamycin. The primers set 2980/2981 used for identification of ermB gene amplified a 688 bp segment. We used the Etest to assess all strains for susceptibility to clindamycin. This study demonstrates that 57% of strains isolated from faecal samples of patients with AAD were highly resistant to clindamycin (minimal inhibitory concentration (MIC) of clindamycin, 256 mg/L) and possessed the ermB gene.

Clindamycin↗
PubMed1993

Comparison of enterotoxin production, cytotoxin production, serogrouping, and antimicrobial susceptibilities of Clostridium difficile strains isolated from AIDS and human immunodeficiency virus-negative patients.

We analyzed and compared Clostridium difficile strains isolated from diarrheic stools of 49 human immunodeficiency virus (HIV)-negative and 50 AIDS patients. Our results suggest that distribution patterns of serogroups are different in these two populations. Serogroup C (which has been previously reported to be very resistant to antimicrobial agents) represents 66.0 and 18.4% of the isolates from AIDS and HIV-negative patients, respectively (P < 0.001); the selection of serogroup C could be explained by multiple antibiotic pressure to which AIDS patients have been subjected.

Acquired Immunodeficiency Syndrome↗
PubMed2000

A chimeric ribozyme in clostridium difficile combines features of group I introns and insertion elements.

CdlSt1, a DNA insertion of 1975 bp, was identified within tcdA-C34, the enterotoxin gene of the Clostridium difficile isolate C34. Located in the catalytic domain A1-C34, Cd/St1 combines features of two genetic elements. Within the first 434 nt structures characteristic for group I introns were found; encoding the two transposase-like proteins tlpA and tlpB nucleotides 435-1975 represent the remainder of a IS605-like insertion element. We show that the entire CdlSt1 is accurately spliced from tcdA-C34 primary transcripts and that purified TcdA-C34 toxin is of regular size and catalytic activity. A search for CdlSt1-related sequences demonstrates that the element is widespread in toxinogenic and non-toxinogenic C. difficile strains, indicating the mobility of CdlSt1. In strain C34, we characterize 10 CdlSt1 variants; all are highly homologous to CdlSt1 (> 93% identity), integrated in bacterial open reading frames (ORFs), show the typical composite structure of CdlSt1 and are precisely spliced from their primary transcripts. CdlSt1-like chimeric ribozymes appear to combine the invasiveness of an insertion element with the splicing ability of a group I intron, rendering transposition harmless for the interrupted gene.

Amino Acid Sequence↗
PubMed1996

Enzyme electrophoresis combined with serogrouping for improved differentiation of Clostridium difficile strains.

We used enzyme electrophoresis to study a set of epidemiologically related and unrelated isolates of Clostridium difficile. The 53 strains belonged to the most frequent serogroups (A1, C, G, H and K). Nine electrophoretic profiles were defined on the basis of five enzymes, and two were characteristic of a single strain. Each serogroup was resolved into two or three different enzyme patterns. By combining the two methods we were able to resolve the strains into 12 types. There was an excellent correlation between enzyme electrophoresis and serogrouping data. This method may be of use in investigating nosocomial transmission.

Bacterial Typing Techniques↗
PubMed1996

Clostridium difficile infection.

The spore-forming anaerobe Clostridium difficile has become a serious enteropathogen. Changes in the composition of natural intestinal flora, mainly due to antibiotic therapy, permit its colonization of, and multiplication in, the colon. The disease is caused by (entero)toxin A and (cyto)toxin B, and infection ranges from asymptomatic carrier state and mild diarrhea to pseudomembranous colitis. The clinical diagnosis is made by observing inflammatory, sometimes bloody, diarrhea and by the colonoscopic detection of epithelial necrosis, ulceration, and, in the advanced state, pseudomembrane formation. The laboratory supports the diagnosis by detecting toxin A and/or B by an enzyme-linked immunoassay with high specificity, but sometimes less sensitivity than with the cytotoxin assay in tissue culture cells. Fecal leukocytes or fecal lactoferrin may be found. Culture for the isolation and identification of toxigenic C. difficile is time consuming but necessary for epidemiological studies. Polymerase chain reaction (PCR) tests have been tested for detection of the toxin B gene directly in stool. Therapy consists of stopping all systemic antibiotic treatment and the use of oral metronidazole or vancomycin. There may be more relapses after vancomycin therapy, and the increasing vancomycin resistance of Enterococcus is worrisome. Prevention, especially of nosocomial spread, requires isolation and enforced handwashing. For epidemiological studies, the bacteria can be typed by molecular DNA analyses, including PCR, protein electrophoresis, and immunological tests.

Antitrichomonal Agents↗
PubMed1991

[The Norrköping study. Cephalosporins are often the implicating factors in Clostridium difficile infections].

In a retrospective study carried out at Norrköping Central Hospital, the incidence of Clostridium difficile-associated diarrhoea and colitis was found to be correlated to in-patient consumption (in terms of defined daily doses) of the implicated anti-microbial agents. The third generation cephalosporin, cefotaxime, was implicated 38 times more often than small spectrum penicillins. In general, the cephalosporins were predominantly responsible, accounting for 46 per cent (67/147) of the episodes but only 12 per cent of overall consumption of antibiotics at the hospital. These findings are in accord with data previously published in the nationwide report by the Medical Product Agency, Uppsala.

Adolescent↗
PubMed1994

Multivalent binding of toxin A from Clostridium difficile to carbohydrate receptors.

A specific monoclonal antibody against toxin A from Clostridium difficile was generated that did not show thermolabile binding. Nonspecific murine monoclonal antibodies bound toxin A at 4 degrees C, but less effectively at 37 degrees C. Nonspecific human monoclonal antibodies did not bind to toxin A at 4 degrees C. Cytotoxic properties of purified toxin A were not inhibited by Bandeiraea simplicifolia lectin. This points to a carbohydrate moiety on the cell surface and a multivalent nonspecific carbohydrate binding ligand on toxin A.

Animals↗
PubMed2004

Bacteriotherapy using fecal flora: toying with human motions.

The intestinal flora may play a key role in the pathogenesis of certain gastrointestinal (GI) diseases. Components of bowel flora such as Lactobacillus acidophilus and Bifidobacterium bifidus have long been used empirically as therapeutic agents for GI disorders. More complex combinations of probiotics for therapeutic bacteriotherapy have also recently become available, however the most elaborate mix of human-derived probiotic bacteria is, by definition, the entire fecal flora. Fecal bacteriotherapy uses the complete normal human flora as a therapeutic probiotic mixture of living organisms. This type of bacteriotherapy has a longstanding history in animal health and has been used sporadically against chronic infections of the bowel, especially as a treatment of last resort for patients with severe Clostridium difficile syndromes including recurrent diarrhea, colitis, and pseudomembranous colitis. Encouraging results have also been observed following infusions of human fecal flora in patients with inflammatory bowel disease, irritable bowel syndrome, and chronic constipation. The therapeutic use of fecal bacteriotherapy is reviewed here and possible mechanisms of action and potential applications explored. Published reports on fecal bacteriotherapy are few in number, and detail the results of small uncontrolled open studies and case reports. Nevertheless, given the promising clinical responses, formal research into fecal bacteriotherapy is now warranted.

Clostridioides difficile↗
PubMed1998

Clostridial pathogenicity in experimental necrotising enterocolitis in gnotobiotic quails and protective role of bifidobacteria.

The pathogenesis of neonatal necrotising enterocolitis (NEC) remains unclear. Gnotobiotic quails fed a lactose diet have been used to investigate the role of clostridial strains originating from faecal specimens of neonates through the intestinal lesions, the changes in microflora balance and the production of bacterial metabolites, i.e., short-chain fatty acids and hydrogen. Bifidobacteria are thought to exert various beneficial effects on host health, including interaction with the colonic microflora. Therefore, it was hypothesised that a protective role could be exercised through bifidobacterial colonisation. A Clostridium butyricum strain (CB 155-3) and a whole faecal flora including three clostridial species (C. butyricum, C. perfringens, C. difficile), each from premature infants suffering from NEC, caused caecal lesions in quails similar to those observed in man, i.e., thickening of the caecal wall with gas cysts, haemorrhagic ulceration and necrotic areas. Conversely, a whole faecal flora including bifidobacteria (identified as Bifidobacterium pseudo-catenulatum) and no clostridia, isolated from a healthy premature infant, was unable to produce NEC-like lesions. When the two clostridial groups were associated with a Bifidobacterium strain (B. infantis-longum, CUETM 89-215, isolated from a healthy infant), bifidobacterial colonisation suppressed all pathological lesions. This study is the first demonstration of a protective role for bifidobacteria against NEC via the inhibition of growth of C. butyricum or the disappearance of C. perfringens. C. difficile was not found to be responsible for the aetiology of the caecal lesions in quails. The main effect of bifidobacteria on lactose fermentation was either a dramatic decrease or a disappearance of butyric acid. The protective role was not associated with changes in H2 production. Therefore, a new step between colonic colonisation and its relevance to NEC is thought to involve the fermentation of unabsorbed lactose into butyric acid at the onset of the disease.

Animals↗
PubMed1994

Comparison of two commercially available enzyme immunoassays for detection of Clostridium difficile in stool specimens.

Clostridium difficile is the cause of most cases of pseudomembranous colitis, the most severe form of antibiotic-associated diarrhea. Rapid diagnosis guides both the treatment and the control of nosocomial spread of infection. Two enzyme immunoassay (EIA) kits developed for the rapid detection of C. difficile toxin A in fecal specimens, Premier (Meridian Diagnostics, Cincinnati, Ohio) and Tox-A test (TechLab, Virginia Polytechnic Institute Research Park, Blacksburg), were evaluated by using 410 fecal specimens. Seventy-six specimens were positive for C. difficile toxin B by the cytotoxin assay (prevalence rate, 19%). The Meridian EIA was positive for 71 of the 76 samples, yielding a sensitivity of 93%. The TechLab EIA detected 75 of the 76 positive samples, yielding a sensitivity of 99%. The Meridian and TechLab EIAs had specificities of 100 and 93%, respectively. These data indicate that both EIAs are suitable alternatives to the cytotoxin assay in routine diagnostic laboratories. However, confirmation of TechLab EIA-positive test results by the cytotoxin assay remains necessary.

Adolescent↗
PubMed1998

Clostridium difficile infection.

Clostridium difficile infection is associated with broad-spectrum antibiotic therapy and is the most common cause of infectious diarrhea in hospital patients. Pathogenic strains of C. difficile produce two protein exotoxins, toxin A and toxin B, which cause colonic mucosal injury and inflammation. Infection may be asymptomatic, cause mild diarrhea, or result in severe pseudomembranous colitis. Diagnosis depends on the demonstration of C. difficile toxins in the stool. The first step in management is to discontinue the antibiotic that caused diarrhea. If diarrhea and colitis are severe or persistent, oral metronidazole is the treatment of choice. Oral vancomycin is also effective, but it is more expensive than metronidazole and its widespread use may encourage the proliferation of vancomycin-resistant nosocomial bacteria. Diarrhea and colitis usually improve within three days after a patient starts taking metronidazole or vancomycin, but 20% suffer a relapse of diarrhea when these agents are discontinued.

Administration, Oral↗
PubMedDate not supplied

Soy fiber delays disease onset and prolongs survival in experimental Clostridium difficile ileocecitis.

Clostridium difficile colitis is a disabling complication in critically ill patients who commonly receive broad-spectrum antibiotics and liquid diets. To date, there is no experimental model specifically designed to investigate the effects of liquid diets on this type of colitis. The addition of fiber to liquid diets normalizes gut structure and improves absorptive function in selected conditions of intestinal dysfunction. The purposes of this study were the following: (1) to develop a reproducible model to examine the interaction of acute C difficile-induced colitis and liquid diets, (2) to determine whether the addition of soy fiber to a liquid diet improves disease, and (3) to investigate possible mechanisms of fiber-mediated disease improvement. Syrian hamsters were pair-fed with either a polymeric liquid diet or the same diet with 1.4% soy fiber for 10 days. Animals were given either clindamycin and C difficile (to produce ileocecitis), or equivalent volumes of saline. Mean survival time and systematic stool examinations for C difficile toxin positivity, liquidity, and percent water were performed to determine the effect of soy fiber on disease. Survival time was prolonged by 34% (p < .05), and C difficile toxin positivity and stool liquidity were significantly reduced (p < .05) with fiber. Additional animals were studied to determine possible mechanisms for improved survival in fiber-supplemented animals. Cecal histology, colonic water absorption, cecal microflora, and gastric to anus transit time were measured in these animals. Colonic water absorption and gastric to anus transit time were significantly increased (p < .05) and decreased (p < .05) with fiber, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Diagnosis and treatment of Clostridium difficile colitis.

Pseudomembranous colitis associated with antibiotic therapy is almost always due to an overgrowth of Clostridium difficile. If untreated, pseudomembranous colitis can lead to severe diarrhea, hypovolemic shock, toxic dilatation of the colon, cecal perforation, hemorrhage, and death. However, C difficile-associated colitis can mimic the more common "benign" antibiotic-associated diarrhea that is not caused by C difficile. An algorithm for diagnosis management of hospitalized patients with antibiotic diarrhea and C difficile colitis is presented in this review. Diagnosis depends on sigmoidoscopy and/or stool tests for C difficile toxins in all patients with antibiotic-associated diarrhea. If the results of these tests are positive, either metronidazole or vancomycin is recommended for treatment of mild illness, and vancomycin is recommended for treatment of severe illness. Oral therapy is always preferred because it is more reliable. In patients with recurrent or relapsing colitis, treatment with either metronidazole or vancomycin is effective for that episode, but novel approaches, such as the oral or rectal introduction of competing nonpathogenic organisms, may prove to be more successful in prevention of relapses.

Anti-Bacterial Agents↗
PubMedDate not supplied

[Severe massive pseudomembranous colitis with a fulminant course].

Pseudomembranous colitis is an inflammatory disease of rectal and colonic mucosa caused by Clostridium difficile produced toxin. The inflammation is produced as the consequence of a non-specific response to several agents. It usually presents with abdominal pain and mild watery diarrhea which used to decrease when removing the antibiotic or when starting the therapy with metronidazole or vancomycin. In aged patients, with severe concomitant diseases, may appear complications such as dehydration, electrolyte imbalance, hypotension and toxic megacolon, which occasionally may lead to fatal outcome. We report the case of a severe pseudomembranous colitis, with a fulminant clinical course, in a patient without a recent antibiotic therapy.

Aged↗
PubMed2004

The cme gene of Clostridium difficile confers multidrug resistance in Enterococcus faecalis.

Antibiotic resistance in C. difficile by efflux has been previously suggested. The genome of C. difficile 630 was screened for sequences encoding putative proteins homologous to NorA from Staphylococcus aureus. Four ORFs homologous to efflux genes were cloned into the pAT79 shuttle vector under the control of transcription and translation signals of Gram-positive bacteria and expressed in Enterococcus faecalis JH2-2 and S. aureus RN4220. One of these sequences, designated cme conferred resistance to ethidium bromide, safranin O, and erythromycin in E. faecalis. The three other ORFs did not confer detectable resistance in both bacteria.

Amino Acid Sequence↗
PubMed2006

Molecular analysis of Clostridium difficile isolates recovered from horses with diarrhea.

Clostridium difficile is an important cause of diarrhea in horses, causing sporadic and epidemic disease of varying severity. This study evaluated the molecular characteristics of 48 C. difficile isolates recovered from diarrheic horses admitted to a veterinary hospital by using PCR-ribotyping and toxin gene profile. Additionally, feces were tested for the presence of C. difficile toxin A/B via enzyme immunosorbant assay (EIA) in 38 horses. The toxin genes tcdA, tcdB and cdtB were present in 27 (56.25%), 35 (72.91%) and 2 (4.1%) strains, respectively. Eight isolates (16.6%) were A(-)B(+) variants. Thirteen of forty-eight isolates (27.0%) did not posses any toxin genes (A(-)B(-)CDT(-)). A positive EIA result was reported in 17 (44%) of the cases. There was no association between the presence of different ribotypes or strains and toxin gene(s) profiles and the clinical outcome.

ADP Ribose Transferases↗
PubMed2002

In vitro activity of 15 antimicrobial agents against clinical isolates of Clostridium difficile in Kuwait.

A total of 73 clinical isolates of Clostridium difficile isolated from stool/rectal swabs of patients admitted to the intensive care units at Mubarak Hospital, Ibn Sina Hospital Burn unit and Haematology wards at the Kuwait Cancer Control Centre, were investigated for their susceptibility to 15 antibiotics using the Etest. Amoxycillin-clavulanic acid, ampicillin, meropenem, metronidazole, penicillin, piperacillin, piperacillin/tazobactam, teicoplanin and vancomycin had excellent activities with MIC(90)s of 0.38, 0.5, 1, 0.19, 1.5, 2, 3, 0.25 and 0.75 mg/l, respectively. Of the 73 C. difficile isolates, 86% were resistant to imipenem (MIC(90) >32 mg/l) and almost 97% were resistant to trovafloxacin (MIC(90)>256 mg/l). Forty eight percent of the isolates were resistant to clindamycin. A total of 18 isolates were highly clindamycin-resistant with an MIC of >256 mg/l; 10 of these were toxin producers. Multiple antibiotic resistance (two or more antibiotics) was noted in 63 isolates. These were more common among the toxigenic strains than the non-toxigenic strains by a ratio of 2.5:1.

Anti-Bacterial Agents↗