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PubMed1992

Systemic and mucosal antibody responses to toxin A in patients infected with Clostridium difficile.

The systemic and mucosal humoral response to toxin A, the primary virulence factor of Clostridium difficile, was measured in sera and intestinal secretions from 21 patients with C. difficile diarrhea, 9 asymptomatic C. difficile fecal excretors, and 10 noncolonized control subjects. Toxin A-specific IgG was higher in convalescent sera of the patients with diarrhea (mean +/- SE, 990 +/- 260 ng/mL) than in acute sera (620 +/- 150 ng/mL), in sera from asymptomatic excretors (410 +/- 140 ng/mL), or control subjects (320 +/- 50 ng/mL; P < .05 convalescent vs. control). The pattern of toxin A-specific serum IgA and intestinal secretory IgA levels was similar to that of serum IgG in these groups. Neutralization of toxin A was demonstrated in 5 of 14 convalescent sera but only 1 of 13 acute sera (P = .04). However, the presence of neutralizing activity was independent of the subsequent clinical response. Therefore, most patients convalescent from C. difficile diarrhea demonstrate systemic and mucosal antibodies to toxin A, but these antibodies following natural infection do not appear to alter the clinical course of C. difficile infection.

Adult↗
PubMed1996

Whole-bowel irrigation as an adjunct to the treatment of chronic, relapsing Clostridium difficile colitis.

We report the successful treatment of two patients with chronic, intractable Clostridium difficile infection using whole-bowel irrigation with a polyethylene glycol solution (Golytely) as adjunctive therapy. Before this treatment, both patients had recurrent symptoms of diarrhea, weight loss, abdominal pain, and documented C. difficile toxin-positive stools despite multiple pharmacologic treatments. Each child was prescribed myriad drug therapies, including vancomycin, metronidazole, bacitracin, and rifampin. Cholestyramine and lactobacillus were also tried alone and in combination with antibiotics. In each case, symptoms recurred shortly after cessation of therapy. Whole-bowel irrigation was subsequently administered until profuse, clear liquid stools were produced. This treatment was followed by a 3-week course of oral vancomycin and lactobacillus. In both cases, the patient became asymptomatic within 3 days of therapy; they have remained symptom-free for 36 and 48 months, respectively. We suggest that whole-bowel irrigation clears active C. difficile organisms, toxins, and spores from the intestine and is effective as an adjunct to routine therapy for chronic, relapsing C. difficile infections.

Anti-Bacterial Agents↗
PubMed1997

Effect of lactulose on short-chain fatty acids and lactate production and on the growth of faecal flora, with special reference to Clostridium difficile.

Lactulose exerts a beneficial effect on hepatic encephalopathy by decreasing toxic short-chain (iC4-nC6) fatty acid (isobutyrate, butyrate, isovalerate, valerate, isocaproate and caproate) production. However, the precise mechanism by which lactulose exerts this effect remains uncertain. This study investigated the effect of lactulose on faecal flora, particularly Clostridium difficile, which produces mostly iC4-nC6 fatty acids. An in-vitro faecal incubation system was used to estimate how lactulose influences production of short-chain (C2-nC6) fatty acids and lactate. Faecal specimens were collected from patients with liver cirrhosis, who carried C. difficile in the colon. Supplementation of lactulose along with blood in faecal specimens decreased iC4-nC6 fatty acids production and increased acetate and lactate production, resulting in increased faecal acidity. These changes were statistically significant when compared with supplementation by blood alone. Quantitative faecal culture demonstrated that lactulose supplementation suppressed the growth of C. difficile and Bacteroides spp. (B. fragilis group), iC4-nC6 fatty acids-producing organisms. These results suggest that decreased faecal levels of iC4-nC6 fatty acids after lactulose supplementation may be related to suppression of iC4-nC6 fatty acids-producing faecal organisms, especially C. difficile.

Aged↗
PubMed2006

Emergence of Clostridium difficile-associated disease in North America and Europe.

The clinical spectrum of Clostridium difficile-associated disease (CDAD) ranges from diarrhoea to severe life-threatening pseudomembranous colitis. Although not always associated with previous antibiotic exposure, it is in the majority of cases. CDAD is recognised increasingly in a variety of animal species and in individuals previously not considered to be predisposed. C. difficile can be transmitted via personal contact or environmentally. The role of patients and healthcare workers who are symptom-free but colonised with C. difficile in the intestinal tract is unclear. C. difficile, with more than 150 PCR ribotypes and 24 toxinotypes, has a pathogenicity locus (PaLoc) with genes encoding enterotoxin A (tcdA) and cytotoxin B (tcdB). Genes for the binary toxin are located outside the PaLoc, but the role of this toxin is unclear. The recently completed genome sequence of C. difficile 630 revealed a large proportion of 11% of mobile genetic elements, mainly in the form of conjugative transposons. Diagnostic assays include tests for the detection of C. difficile products or genes and culture methods for isolation of a toxin-producing bacterium. Enzyme immunoassays to detect toxin in faeces are widely available, with varying sensitivities and specificities. Despite practical drawbacks and sensitivity less than 100%, the cell cytototoxicity assay is still considered to be the standard. Rapid diagnostic assays are available on a limited scale and require much improvement. Molecular tests enable the detection of carriers of toxigenic and non-toxigenic strains, as does culture. It is highly recommended to culture C. difficile from toxin-positive faeces samples and to store isolates for future characterisation and typing. The financial impact of CDAD on the healthcare system is substantial (5-15,000 euro/case in England and $1.1 billion/year in the USA). Assuming a European Union population of 457 million, the potential cost of CDAD can be estimated to be 3000 million euro/year, and is expected to almost double over the next four decades. In North America, increasing rates of CDAD have been reported in Canada and the USA since March 2003, involving a more severe course, higher mortality, increased risk of relapse and more complications. This increased virulence is presumably associated with higher levels of toxin production by fluoroquinolone-resistant strains belonging to PCR ribotype 027, pulsed-field gel electrophoresis (PFGE) type NAP1, REA (restriction endonuclease analysis) type BI and toxinotype III. In Europe, outbreaks of CDAD due to the new, highly virulent strain of C. difficile PCR ribotype 027, toxinotype III have been recognised in 75 hospitals in England, 16 hospitals in The Netherlands, 13 healthcare facilities in Belgium and nine healthcare facilities in France. These outbreaks are very difficult to control, and preliminary results from case-control studies indicate a correlation with fluoroquinolones and cephalosporins. Information concerning community-acquired cases of ribotype 027 is lacking, and data concerning its incidence in nursing homes are limited. European countries should first develop early-warning and response capabilities at a national level. Depending on the nature of the notifications received, countries should implement laboratory-based or patient-based surveillance systems in specific, targeted populations.

Animals↗
PubMed1991

Binding kinetics of Clostridium difficile toxins A and B to intestinal brush border membranes from infant and adult hamsters.

This study was undertaken to determine if the relative resistance of neonates and infants to Clostridium difficile-associated intestinal disease can be related to age-dependent differences in intestinal receptors for C. difficile toxins A and B. Brush border membranes (BBMs) from the small intestines of adult and infant hamsters were examined for their ability to bind radiolabeled toxins A and B. [125I]toxin A bound to both infant and adult hamster BBMs at physiological temperature, whereas [125I]toxin B did not bind to the BBMs under any of the conditions examined. The number of [125I]toxin A molecules bound at saturation was approximately 4 x 10(10) per micrograms of membrane protein for adult BBMs and 1 x 10(11) per micrograms of membrane protein for infant BBMs. Scatchard plot analysis suggested the presence of a single class of toxin A binding sites on both infant and adult hamster BBMs. Maximal binding capacity and Kd values were 0.63 pmol/mg of protein and 66.7 nM, respectively, for the infant BBMs, and 0.24 pmol/mg of protein and 27 nM, respectively, for the adult BBMs. Sodium dodecyl sulfate-polyacrylamide gel electrophoretic analyses of extracted BBM proteins revealed differences in the proteins of infant and adult BBMs. However, there were not any detectable differences in the protein bands which bound [125I]toxin A between infant and adult hamsters. The results from these investigations indicate that differences in the binding kinetics of toxins A and/or B to infant and adult hamster BBMs do not account for the observed differences in their susceptibility to C. difficile-associated intestinal disease.

Age Factors↗
PubMed2006

Clostridium difficile infection in patients discharged from US short-stay hospitals, 1996-2003.

US hospital discharges for which Clostridium difficile-associated disease (CDAD) was listed as any diagnosis doubled from 82,000 (95% confidence interval [CI] 71,000-94,000) or 31/100,000 population in 1996 to 178,000 (95% CI 151,000-205,000) or 61/100,000 in 2003; this increase was significant between 2000 and 2003 (slope of linear trend 9.48; 95% CI 6.16-12.80, p = 0.01). The overall rate during this period was severalfold higher in persons >65 years of age (228/100,000) than in the age group with the next highest rate, 45-64 years (40/100,000; p < or = 0.001). CDAD appears to be increasing rapidly in the United States and is disproportionately affecting older persons. Clinicians should be aware of the increasing risk for CDAD and make efforts to control transmission of C. difficile and prevent disease.

Adolescent↗
PubMed2000

[Diagnosis of Clostridium difficile infection in pseudomembranous colitis].

C. difficile is known as the main cause of pseudomembranous colitis, however, some individuals may be asymptomatically colonized. In this paper two patients with diarrhoea had three respectively five negative stool cultures. Endoscopically, one patient had severe colitis consistent with both pseudomembranous colitis and inflammatory bowel disease. In the other case the endoscopic findings were typical for pseudomembranous colitis. In both cases there were positive cultures for C. difficile from biopsies from colon-plaques. We find that culture of biopsy of a colon-plaque may contribute to the detection of C. difficile infection in patients with negative stool cultures.

Aged↗
PubMed2003

Prevalence of asymptomatic Clostridium difficile colonization in a nursing home population: a cross-sectional study.

OBJECTIVE: We conducted a cross-sectional study to determine the prevalence of asymptomatic Clostridium difficile in a nursing home population. METHODS: Inclusion criteria for the study required that the subjects be residents of the facility for more than 1 month. Exclusion criteria included: (1) patients who developed C. difficile infection within 2 months prior to stool collection; (2) metronidazole or vancomycin therapy within 2 months prior to stool collection; (3) past surgical history of colectomy; and (4) possible signs and symptoms of active C. difficile infection. RESULTS: The prevalence of asymptomatic C. difficile infection in this population was 5%. There was no significantly higher prevalence of asymptomatic C. difficile based on age, race, length of stay, gender, diabetes, renal failure, history of cancer, recent antibiotic use, gastric tube, histamine2 blocker/proton pump inhibitor use, Foley catheter, or dementia. CONCLUSIONS: The prevalence of asymptomatic C. difficile in this population is similar to previously studied populations. Further research should follow a cohort of asymptomatic individuals with C. difficile to determine if colonization may be protective against symptomatic infection.

Clostridioides difficile↗