The Spectrum of Pseudomembranous Enterocolitis and Antibiotic-Associated Diarrhea

Abstract

Pseudomembranous (entero)colitis is primarily caused by Clostridium difficile infection. The most common predisposing factor is prior use of antibiotics, including vancomycin and metronidazole, which themselves are therapy for C difficile colitis. Other risk factors have also been described. The presence of C difficile in the gastrointestinal tract leads to a spectrum of manifestations from the asymptomatic carrier state to fulminant colitis. Successful treatment of C difficile colitis requires prompt treatment with appropriate antibiotics, withdrawal of the suspected predisposing antibiotics, and, in rare cases, total colectomy. Preventive measures of adequate infection control and judicious use of antibiotics are necessary means in attempting to control the spread of C difficile infection. Attempts at making an effective human vaccine are currently under way.

Germination of spores of Clostridium difficile strains, including isolates from a hospital outbreak of Clostridium difficile-associated disease (CDAD)

“…CDAD is thought to be initiated by the ingestion of C. difficile spores, which then germinate, grow and produce virulence factors that cause severe damage to the intestinal epithelium, leading to an acute inflammatory response (Borriello, 1998;Hurley & Nguyen, 2002). To understand the initial stages of pathogenesis of CDAD, we have characterized the germination of five CDAD isolates (McEllistrem et al, 2005) and one laboratory strain of C. difficile.…”

“…However, CDAD symptoms affect primarily the large intestine and rarely the small intestine (Hurley & Nguyen, 2002), perhaps because either most C. difficile spores germinate primarily in the large intestine due to the presence of K + ions or spores do germinate in early segments of the GI tract but do not outgrow appreciably in the small intestine and only outgrow, colonize, release toxins (TcdA and TcdB) and cause CDAD symptoms in the large intestine.…”

“…CDAD generally occurs subsequent to a course of antibiotic treatment, which disrupts the normal colonic flora and allows the ingested C. difficile spores to germinate, outgrow and proliferate rapidly, filling empty niches (Kelly et al, 1994;Kelly & LaMontt, 1998). During vegetative growth, C. difficile cells produce two major toxins, TcdA and TcdB (Borriello et al, 1990;Voth & Ballard, 2005), which cause a wide spectrum of nosocomial diseases, ranging from mild, self-limiting diarrhoea to serious and life-threatening pseudomembranous colitis and toxic megacolon (Borriello, 1998;Hurley & Nguyen, 2002).…”

Products of Metabolism of the Intestinal Microflora: Can We Use the Selective Correction?

“…Парадоксально, что антибиотики могут приводить к раз-растанию таких опасных патологических микроорганиз-мов, как грибы Candida, Clostridium difficile и др. [7].…”

Characteristics of Clostridium difficile infection in a high complexity hospital and report of the circulation of the NAP1/027 hypervirulent strain in Colombia

“…La toxina A es una enterotoxina que rompe las uniones intercelulares de los enterocitos y facilita el ingreso de la toxina B, la cual activa los macrófagos y los mastocitos que, a su vez, generan un aumento de la permeabilidad epitelial, de la producción de citocinas, la infiltración de neutró-filos, la producción de intermediarios de especies reactivas del oxígeno, la activación de mastocitos, la producción de sustancia P y el daño directo en la mucosa. En cuanto a la toxina binaria, su mecanismo patogénico aún no está del todo dilucidado, pero al parecer incrementa la adhesión de las cepas de C. difficile y actúa a nivel del citoesqueleto de la célula, provocando una mayor pérdida de líquidos, por lo que las cepas portadoras de dicha toxina se han asociado a una mayor virulencia (4,5,(7)(8)(9).…”