Comparative histopathology of intestinal infections

Abstract

Intestinal infections are characterized by a range of histologic changes. Some examples (moving progressively deeper into the tissue from the intestinal lumen) are: 1) Enterotoxigenic E. coli infections are characterized by layers of E. coli adherent to villous epithelium, usually with little or no apparent structural damage to the mucosa. 2) The term enteropathogenic E. coli infection designates a disease characterized by E. coli attached intimately to the epithelial cell surface membrane with effacement of brush border microvilli. 3) Rotavirus infections are characterized by destruction of villous epithelial cells. Parvovirus infections are characterized by destruction of crypt epithelial cells. 4) Some intracellular infections with Campylobacter-like organisms are characterized by epithelial cell hyperplasia. 5) Hemorrhagic colitis in humans, caused by enterohemorrhagic E. coli strains, is characterized by mucosal hemorrhage and edema indicative of vascular necrosis. 6) Most of these lesions are accompanied by some degree of inflammation. Neutrophils and lymphocytes mediate some of the structural and functional changes characteristic of these infections. Some changes are mediated directly by microbial products. Additional examples of the complexity of these diseases are: 1) Edema disease of swine is characterized both by adherent E. coli and vascular necrosis (each process mediated by a different bacterial virulence attribute). 2) Rotavirus infections are characterized both by destruction of villous epithelial cells and compensatory hyperplasia of crypt epithelial cells. 3) There is suggestive evidence that enterohemorrhagic E. coli infections may involve: a) destruction of epithelial brush border by attaching - effacing E. coli, b) neutrophil mediated epithelial cell destruction, c) Shiga-like toxin mediated epithelial cell destruction and d) Shiga-like toxin mediated vascular necrosis which in turn causes ischemic damage to epithelium.