Enteropathogenic E. coli (EPEC) organisms are characterized by their ability to produce attaching and effacing (A/E) lesions in which bacteria attach tightly to the enterocyte apical membranes and cause local loss (i.e., effacement) of the microvilli. The proteins necessary for creating A/E lesions are all encoded by a large genomic pathogenicity island, the locus of enterocyte effacement (LEE). This locus also encodes a type III secretion system, similar to that in Shigella, that injects bacterial effector proteins into the epithelial cell cytoplasm. EPEC can cause endemic diarrhea as well as diarrheal outbreaks particularly in children younger than 2 years of age.
Enterohemorrhagic E. coli (EHEC) organisms are categorized as O157:H7 and non-O157:H7 serotypes. Outbreaks of E. coli O157:H7 in developed countries have been associated with the consumption of inadequately cooked ground beef, milk, and vegetables. Both O157:H7 and non-O157:H7 serotypes produce Shiga-like toxins and can cause dysentery. They can also trigger hemolytic-uremic syndrome (Chapter 14).
Enteroinvasive E. coli (EIEC) organisms resemble Shigella bacteriologically but do not produce toxins. They invade the gut epithelial cells and produce a bloody diarrhea.
Enteroaggregative E. coli (EAEC) organisms attach to enterocytes by adherence fimbriae. Although they produce LT and Shiga-like toxins, histologic damage is minimal.
Salmonella species, which are members of the Enterobacteriaceae family of gram-negative bacilli, are divided into Salmonella typhi, the causative agent of typhoid fever and nontyphoid Salmonella strains that cause gastroenteritis. Nontyphoid Salmonella infection usually is due to Salmonella enteritidis; more than 1 million cases occur each year in the United States, which result in 2000 deaths; the http://ebooksmedicine.net prevalence is greater in many other countries. Infection is most common in young children and older adults, with a peak incidence in summer and fall. Transmission usually is through contaminated food, particularly raw or undercooked meat, poultry, eggs, and milk.
Very few viable Salmonella organisms are necessary to cause infection, and the absence of gastric acid, as in individuals with atrophic gastritis or those on acid-suppressive therapy, further reduces the required inoculum. Salmonellae possess virulence genes that encode a type III secretion system capable of transferring bacterial proteins into M cells and enterocytes. The transferred proteins activate host cell Rho GTPases, thereby triggering actin rearrangement and bacterial uptake into phagosomes where the bacteria can grow. Salmonellae also secrete a molecule that induces epithelial release of a chemoattractant eicosanoid that draws neutrophils into the lumen and potentiates mucosal damage. Stool cultures are essential for diagnosis.