| Verotoxin-producing E. coli | |
|---|---|
| Classification and external resources | |
| ICD-10 | A04.3 |
| ICD-9 | 008.04 |
Verotoxin-producing Escherichia coli comprise strains of the bacterium Escherichia coli that, when infecting humans, have been linked with the severe complication hemolytic-uremic syndrome (HUS). They are known by a number of names, including enterohemorrhagic E. coli (EHEC), Shiga-like toxin-producing E. coli (STEC or SLTEC), hemolytic uremic syndrome–associated enterohemorrhagic E. coli (HUSEC) and verocytotoxin- or verotoxin-producing E. coli (VTEC).[1]
All these E. coli strains produce Shiga-like toxin (also known as verotoxin), a major cause of foodborne illness. These are distinguished from other pathotypes of intestinal pathogenic E. coli including enterotoxigenic E. coli (ETEC), enteropathogenic E. coli (EPEC), enteroinvasive E. coli (EIEC), enteroaggregative E. coli (EAEC), and diffusely adherent E. coli (DAEC).[2]
The best known of these strains is O157:H7, but there are non-O157 strains which cause an estimated 36,000 illnesses, 1,000 hospitalizations and 30 deaths in the United States yearly.[3] Food safety specialists recognize "Big Six" strains; O26, O45, O103, O111, O121, and O145.[3] A 2011 outbreak in Germany was caused by another STEC, O104:H4. This strain has both enteroaggregative and enterohemorrhagic properties. Both the O145 and O104 strains can cause hemolytic-uremic syndrome, the former strain shown to account for 2% to 51% of known HUS cases; it has been estimated that 56% of such cases are caused by O145 and 14% by other EHEC strains.
EHEC that induces bloody diarrhea leads to HUS in 10% of cases. The clinical manifestations of post-diarrheal HUS include acute renal failure, microangiopathic hemolytic anemia, and thrombocytopenia. The verocytotoxin (shiga-like toxin) can directly damage renal and endothelial cells. Thrombocytopenia occurs as platelets are consumed by clotting. Hemolytic anemia results from intravascular fibrin deposition, increased fragility of red blood cells, and fragmentation.[2]
Antibiotics are of questionable value and have not shown to be of clear clinical benefit. Antibiotics that interfere with DNA synthesis such as fluoroquinolones have been shown to induce the Stx-bearing bacteriophage and cause increased production of toxins.[4] Attempts to block toxin production with antibacterials which target the ribosomal protein synthesis are conceptually more attractive. Plasma exchange offers a controversial but possibly helpful treatment. The use of antimotility agents (medication that suppresses diarrhea by slowing bowel transit) in children under 10 years of age or in elderly patients should be avoided as it increases the risk of HUS with EHEC infections.[2]
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