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At least 37 records · Page 2Linked to original sources
PubMed1998

[Some aspects of the Clostridium difficile infection].

Clostridium difficile is now regarded as the most common nosocomial enteric pathogen. C. difficile infection has a wide spectrum of a clinical presentation ranging from asymptomatic carriage to the fulminant colitis. Antibiotic therapy is the most important risk factor in pathogen contagion, however other factors are also involved. Typical pathophysiology: 1. alteration of the indigenous colonic flora by antibodies, 2. ingestion of spores, 3. colonization by Clostridium difficile, 4. production of its toxins. Both entherotoxin A and cytotoxin B are active in human colon. The mode of action of these toxins is already quite well known. The main treatment includes withdrawal of the inducing agents, supported occasionally by oral Vancomycin and Metronidazole. Relapse is a major complication.

Anti-Bacterial Agents↗
PubMed1989

Maternal deaths associated with Clostridium sordellii infection.

Clostridium sordellii is a common soil and enteric bacterium that is infrequently recovered from the vagina. We describe three women in which C. sordellii caused puerperal infection and a distinctive and lethal toxic shock-like syndrome. Patients were less than 1 week post partum and each had a single, limited focus of infection including infection associated with a retained vaginal sponge, a cesarean section operative site, and endometritis. Each patient had a distinctive course characterized by sudden onset of clinical shock marked by severe and unrelenting hypotension associated with marked, generalized tissue edema and "third spacing" with increased hematocrit, presence of marked leukemoid reaction with total neutrophil counts of 84,000/mm3, 66,000/mm3, and 93,600/mm3, absence of rash or fever, limited or no myonecrosis, and a rapid and uniformly lethal course. Hypoalbuminemia was also noted. Similar findings were noted in prior isolated reports of C. sordellii-mediated postpartum or surgical infection. Treatment of animals with C. sordellii or closely related C. difficile toxins produces similar findings. We suggest that localized infection with toxin-producing strains of C. sordellii can produce a rapidly lethal toxic shock-like syndrome. Further study and earlier recognition of this syndrome may be life-saving in other patients.

Adult↗
PubMed2003

[Gene-engineering approach for the production of A and B toxin fragments for diagnostic and immunotherapeutic use in Clostridium difficile infection].

Clostridium difficle is a causative agent of severe and difficult-to-diagnose human infections. Toxins A and B, which modify the RAS-like proteins of eukaryotic cells, are the major factor in the pathogenicity of the discussed causative agent. These very toxins are considered as the key components of the developed diagnostic and therapeutic-and-preventive preparations. The C-terminal fragments of toxins A and B as well as hybrid products, consisting of fragments of both toxins, were cloned, within the present case study, by using the pET28 plasmid vector. The recombinant plasmids were transformed into strains Escherichia Coli BL21 (DE3), and they were used later to produce the appropriate proteins. The purified protein preparations were isolated from the ultrasound bacterial-cell lysate by using the method of metal-affinity chromatography to be used later in the production of hyper-immune rabbit sera.

Animals↗
PubMed1996

Immune response to Clostridium difficile infection.

Clostridium difficile produces two toxins (A and B) which cause antibiotic-associated diarrhoea and pseudomembranous colitis. One of the most puzzling aspects of C. difficile infection is the wide spectrum of clinical presentation which ranges from asymptomatic carriage to fulminant, life-threatening colitis. This review examines the hypothesis that immune responses to C. difficile underlie these dramatic variations in disease presentation and course. Animals can be protected from C. difficile colitis by passive or active immunization against toxins A and B. Human antibody responses to these toxins are evident in approximately 60% of the general population. A number of clinical studies indicate that antitoxin responses in both serum and intestinal secretions may be protective whereas an inadequate immune response predisposes to severe or recurrent C. difficile diarrhoea. Thus there is now considerable interest in developing methods for passive and active immunization to combat this prevalent nosocomial intestinal pathogen.

Animals↗
PubMed2000

Update on Clostridium difficile infection.

Clostridium difficile is a major cause of antibiotic-associated diarrhea in hospital and community settings, spreading endemic and epidemic disease in developed and developing areas throughout the world. Its toxins A and B cause epithelial disruption, inflammation, and secretion. Diagnosis of infection with C. difficile is based on appropriate clinical presentation and demonstration of the presence of either toxin A or B, or both. Established treatment is still predominantly metronidazole and vancomycin. The association of antibiotic therapy with recurrent disease and antimicrobial resistance, especially vancomycin-resistant enterococci, highlights the need for new approaches to managing C. difficile infection.

Anti-Bacterial Agents↗
PubMed1994

[Nosocomial acquisition of Clostridium difficile infections].

Clostridium difficile (CD) is associated with diarrhea in hospital patients receiving antibiotic therapy and may be nosocomially acquired. An outbreak of CD diarrhea was observed among elderly patients in acute hospital and geriatric rehabilitation wards. All but 1 patient presenting with diarrhea had a toxin-positive stool culture. Of patients with CD toxin-positive cultures, 4 died, 5 recovered completely and 1 became a chronic carrier. Effective preventive measures are needed to reduce nosocomial acquisition of CD.

Aged↗
PubMed1998

Community-acquired Clostridium difficile infection.

Clostridium difficile-associated disease (CDAD) is primarily a nosocomial condition. Community-acquired disease has been reported but the incidence is felt to be low and the rate of disease resulting in hospitalization is reported as negligible. We recently experienced a 6-month outbreak of CDAD (January to June 1995): 139 patients were involved and four deaths were attributable to pseudomembranous colitis. Early in the outbreak period we were aware that many new admissions presented with C. difficile cytotoxin B positive diarrhoea: in some cases this was the sole reason for hospitalization. This observation forms the basis of this report.

Adult↗
PubMed2001

Mathematical modeling of Clostridium difficile infection.

Clostridium difficile diarrhea is a major cause of morbidity and mortality in hospitals. However, the number of cases in an outbreak is usually relatively small. This precludes many traditional statistical methods of modeling epidemics. Stochastic models are designed to deal with small numbers and are promising methods of understanding C. difficile epidemiology. This is illustrated by a reversible jump Markov chain Monte Carlo model based on the herd immunity hypothesis of C. difficile outbreaks.

Clostridioides difficile↗
PubMed2005

Intravenous immunoglobulin for resistant Clostridium difficile infection.

Clostridium difficile (CD)-associated diarrhoea and colitis may relapse in up to 20% of treated patients. We present a patient who failed to respond over a 6-month period to treatment either singly or in combination with metronidazole, vancomycin, rifampicin, cholestyramine and probiotics. Her diarrhoea rapidly resolved after a 3-day course of intravenous immunoglobulin. This treatment may compensate for a failed immune response to CD toxin and should be considered for relapsing CD-associated diarrhoea where there is no response to conventional treatment strategies.

Clostridioides difficile↗