Probiotics for the Prevention and Treatment of Clostridium difficile in Older Patients

Jasmin Islam; Jonathan Cohen; Chakravarthi Rajkumar; Martin J. Llewelyn

Disclosures

Age Ageing. 2012;41(6):706-711. 

In This Article

Pathogenesis of CDI

CDI occurs when changes in gut physiology and microflora allow ingested spores to reach the colon, germinate and become established through specific adhesins. Diarrhoea is toxin mediated with disruption to the colonic epithelial integrity resulting in epithelial detachment, fluid accumulation and tissue destruction.[14] The two C. difficile Toxins, A and B, are very similar and apparent differences in function may relate to receptor specificity.[15] Toxin A may not be necessary for virulence since virulent Toxin A–B + strains are now well described.[16] Antibodies to these toxins provide some protection from disease, and only around one-third of patients develop symptoms after infection.[17,18] Strains such as the 'hypervirulent' 027 strains produce larger quantities of Toxins A and B but also synthesise an additional 'Binary' Toxin the role of which is not established.

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