Pathogenesis of infectious diarrhea: GUT PHYSIOLOGY Part 7

GUT PHYSIOLOGY Part 7EAEC and DAEC: In comparison with the previously discussed E coli pathotypes, the pathogenesis of EAEC and DAEC infections are much less well understood. The characteristic histopathological feature induced by EAEC is the aggregation of bacteria entrapped within a mucous gel, accompanied, not surprisingly, by pitted goblet cells. In volunteer studies, diarrhea was predominantly mucoid. Genes encoding EAEC adhesins and EAST1 have been identified on a 60 MDa plasmid. Another cytotoxin has been recognized of as yet unknown biological significance. Even less is known about the pathogenesis of DAEC infection, but the separation of DAEC into a separate subclass of diarrheagenic E coli is apparently confirmed by the isolation of genes that mediate the diffuse monolayered type of adherence.

Salmonella species: In this section, Salmonella species are dealt with under two headings, which reflects a recent perception that there are at least two invasive biotypes of this pathogen that cross conventional serotypic boundaries. Salmonella species are an example of a diarrheagenic pathogen, some strains of which actually cause the detachment of epithelial cells. Arising from combined quantitative and electron microscopic studies of the invasiveness of various Salmonella strains, both in vivo in rabbits, pigs and calves, and in vitro in explants of rabbit terminal ileum, it is clear that Salmonellae species can be grouped as histotoxic or nonhistotoxic according to how they initially interact with the gut epithelium. A summary of the findings from our laboratory is given below. buy ortho tri-cyclen online

Histotoxic Salmonella species: The main feature of the early damage to epithelia caused by histotoxic Salmonella species is a toxin-mediated detachment of enterocytes that is preceded by cleavage of tight junctions. This leads to the release of microvilli-bearing cells that degenerate rapidly into spherical highly vacuolated entities. The toxin may be an intracellularly acting cytotoxin that causes disruption of tight junctions and subsequent intracellular disorganization from the inside. Alternatively, it may act externally on tight junctions, with subsequent cytopathic changes occurring as a result of highly differentiated enterocytes being removed from their normal environment. Later in the infection, bac-teria-laden cells that did not appear to be extensively vacuolated, were seen being shed, perhaps indicating that toxin activity is expressed intralumenally rather than intracellularly. Similar lesions were produced in rabbit tissues challenged in vivo and in vitro with live histotoxic Salmonella typhimurium and Salmonella dublin strains. Sterile supernates from rabbit gut challenged in vitro with histotoxic S typhimurium strain GM3 induced an almost identical picture of epithelial disintegration when added to fresh tissue from the same animal. In calves and pigs, histotoxic S dublin strain 3246 caused extensive tissue damage to both absorptive epithelium (AE) and follicle-associated epithelium (FAE). Salmonella serotype choleraesuis was not histotoxic in any experimental setting. These observations are of crucial importance in attempting to understand the pathogenesis of Salmonella infection. By virtue of their ability to denude epithelia, these organisms open up new routes of invasion and tissue transmigration. It was not difficult to demonstrate histotoxic S dublin inside disintegrating cells near vascular elements of infected bovine tissues.

This entry was posted in Diarrhea and tagged Bibrio cholerae, Clostridium difficile, Diarrhea, Escherichia coli, Shigella dysenteri.