Su C, Brandt LJ
Escherichia coli O157:H7 infection in humans (REVIEW)

Ann Int Med (Nov) 123:698-714 1995

This is a review paper about complications of infection with E. Coli O157:H7, including bloody diarrhea, thrombotic thrombocytopenic purpura (TTP), and hemolytic uremic syndrome (HUS). The pathogenetic properties of O157:H7 are linked to secretion of one or more Shiga-like toxins (so-named because of a similarity to toxins secreted by Shigella). Other E. Coli strains, however, also secrete similar toxins and can cause TTP and HUS. Clinical manifestations of infection include severe abdominal cramps, nausea, vomiting, and watery, then bloody diarrhea. Many infected patients are asymptomatic. Bloody diarrhea does not always progress to HUS, and HUS can occur in the absence of a bloody diarrhea prodrome. Lab findings include leukocytosis, ileus, and often "thumbprinting" on barium enema, a sign otherwise suggestive of ischemic colitis. The most severe disease is in the cecum and right colon.

E.Coli O157:H7 is the most important etiologic agent for typical HUS, being isolated from 45-75% of cases. Among patients infected with O157:H7, HUS develops in 2-7%. Other strains of Shiga-like toxin producing E.Coli may be more common in other countries, e.g., Argentina. Very young or old age are predisposing causes, as is prolonged use of antimotility agents. TTP has been reported after infection with O157:H7 in adults, but not in children.

Epidemiology: O157:H7 is found in 2% of all diarrheal infections, and in 15-36% of patients with bloody diarrhea. Cases occur worldwide, and incidence appears to be increasing, especially of HUS. Peak incidence is in summer. Food borne transmission is the most important means of infection, esp. undercooked hamburger meat. Other meats and even unpasteurized milk and apple cider have been implicated was well. Beef and dairy cattle are thought to be the principal reservoir for O157:H7. Secondary person-to-person contact may be an important method of spread in institutions and day care centers.

E.Coli O157:H7 secrete two type of Shiga-like toxins, I and II. The former is quite similar to true Shiga toxin. They both bind to a receptor globotriaosyl ceramide, which is highly expressed in renal cortex. Shiga II toxin appears to be most closely linked to HUS. However, in vitro, Shiga I toxin is directly toxic to endothelial cells and products thrombotic microangiopathic like lesions. The proposed pathogenesis is toxin-induced injury to endothelial cells, increased platelet aggregation, intravascular thrombus formation, and ischemic injury. There is some evidence in animals (pigs) for pathogenesis due to non-toxin mediated mechanisms as well.

Methods of detection include culturing in special sorbitol- McConkey agar, Sorbito-negative colonies can by serotyped with O157 and H7 antisera. Shiga-like toxin detection requires cultured cells, but new methods including immunospecific assays and genetic probes are becoming available. Increases in plasma neutralizing antibodies can also be used.

No treatment has been shown to be effective, and antibiotics may worsen the course by eliminating competing bowel flora or to sublethal damage to the bacteria, causing liberation of Shiga-like toxins. Prevention includes proper cooking of meat and pasteurization of milk. Infection control measures should be taken when an epidemic of bloody diarrhea is found in a closed setting such as a nursing home or day care center. (Daugirdas)

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ARF etiology : Hemolytic/uremic syndrome and TTP