Clostridium difficile as an inducer of inflammatory diarrhea

Abstract

Clostridium difficile has been pointed out as an important agent of diarrheal diseases associated with antibiotic use. However, due to its complexity, the physiopathology of these diseases is only partially elucidated, although a series of scientific works has demonstrated the importance of toxins A and B in the pathogenesis of the inflammatory diarrhea induced by this microorganism. The inflammatory mechanisms involved in the biological activities of these toxins are complex. There are some studies demonstrating that toxin B has no enterotoxic activity in vivo. However, this toxin causes dose-dependent eletrophysiologic and morphologic modifications of human colonic mucosa in vitro. In addition, toxin B stimulates the synthesis of potent inflammatory mediators by monocytes and macrophages. The effects provoked by toxin A on the intestinal mucosa are quite evident and are characterized by intense fluid secretion and by inflammatory cell accumulation, such as macrophages, mast cells, lymphocytes and neutrophils, with the consequent release of mediators such as prostaglandins, leukotrienes, platelet activating factor, nitric oxide and cytokines.