ENTEROHEMORRHAGIC E. coli (EHEC)
EHEC disease and the accompanying hemolytic uremic syndrome (HUS) are the result of consumption of products from animals colonized with EHEC strains. It is also clear from secondary cases in families during outbreaks that person-to-person transmission also occurs. This disease occurs more in developed rather than in developing countries.
EHEC was first recognized in the early 1980s when outbreaks of HUS (hemolytic anemia, renal failure, and thrombocytopenia) were linked to a single E. coli serotype, O157:H7. Since then EHEC disease has emerged as an important cause of bloody diar-rhea in industrialized nations and retained a remarkable but not exclusive relationshipwith the O157:H7 serotype, particularly in North America. Regional and national out-breaks associated with unpasteurized juices and hamburger have caught the attention of the public, the press, and the government.
The emergence of EHEC is related to its virulence , low infecting dose, common reservoir (cattle), and changes in the modern food processing industry that pro-vide us with fresher meat (and bacteria). The low infecting dose, estimated at 100 to 200 organisms, is particularly important. This is a level where food need not come directly from the infected animal, only be contaminated by it. For example, large modern meat processing plants can mix EHEC from colonized cattle at one ranch into beef from hun-dreds of other farms and quickly ship it all over the country. Therefore, the worst out-breaks have been seen in countries with the most advanced food production systems. If the organisms are ground into hamburger, an infecting dose of EHEC may remain even after cooking if the meat is left rare in the middle. Unpasteurized milk carries an obvious risk but fruits and vegetables have also been the source for EHEC infection. In these in-stances the EHEC from the manure of cattle grazing nearby has contaminated these prod-ucts in the field. The bacterial dose from a few “drop” apples (those picked up from the ground) included in a batch of cider has been enough to cause disease.
The distinguishing feature of the EHEC is the production of both Shiga toxins and the A/E lesions described above for EPEC. Another difference between EHEC and EPEC is that EHEC primarily attacks the colon while EPEC infects the small intestine. The multi-ple extraintestinal features such as HUS appear to be the result of circulating Shiga toxin. The interaction of EHEC with enterocytes is much the same as EPEC, except the EHEC strains do not form localized microcolonies on the mucosa. The outer membrane protein intimin mediates adherence and the contact secretion system injects the E. coli secretion proteins, which cause alterations in the host cytoskeleton. The genes for these properties are also found in a PAI.
The A/E features alone are sufficient to cause nonbloody diarrhea. Shiga toxin pro-duction causes capillary thrombosis and inflammation of the colonic mucosa, leading to a hemorrhagic colitis. Although it has not been detected in the blood of human cases, Shiga toxin is presumed to be absorbed across the denuded intestinal mucosa. Circulating Shiga toxin binds to renal tissue where its glycoprotein receptor is particularly abundant, caus-ing glomerular swelling and the deposition of fibrin and platelets in the microvasculature. How Shiga toxin causes hemolysis is less clear; perhaps the erythrocytes are simply dam-aged as they attempt to traverse the occluded capillaries. The strong association between EHEC disease and the O157:H7 serotype suggests that EHEC are more than just Shiga toxin – producing EPEC. The O157:H7 strains invariably have a large plasmid which may contain other virulence genes. Cases and outbreaks caused by Shiga toxin – producing E. coli of other serotypes may be on the rise and are common in some countries. Howthey differ from O157:H7 EPEC remains to be seen.