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.
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ARF etiology :
Hemolytic/uremic syndrome and TTP