Diagnosis of Shiga toxin producing Escherichia coli infection

Escherichia coli (E. coli) is an important member of the


normal intestinal microflora of humans and other mammals.

However, E. coli is more than just harmless intestinal inhabitant;

it can also be a highly pathogenic. Several different

E. coli strains cause diverse intestinal and extraintestinal diseases

by means of virulence factors that affect a wide range

of cellular processes [1].

Shiga toxin producing E. coli (STEC) is an important

emerging food borne pathogen. It has been associated with

bloody and non-bloody diarrhea, hemorrhagic colitis hemolytic uremia syndrome (HUS) and thrombotic thrombocytopenic


purpura. The cattle’s have been shown to be the major

reservoir of STEC are foods such as ground beef and milk [2].

The term verocytoxin e producing E. coli was derived form

the observation that these strain produce a toxin with a profound

and irreversible cytopathic effect on Vero cells (African

green monkey kidney) [3]. An a alternative nomenclature is

Shiga toxin-producing E. coli STEC which reflects the fact

that one of the cytotoxins produced by these organisms is essentially

identical at the genetic and protein levels to Shiga

toxin (stx) produced by Shigella dysenteriae 1 [4].

Isolation and recognition of the prominent Shiga toxin- producing

strains of Escherichia coli serovar O157:H7 can be

confirmed easily by their late fermentation of sorbitol and

lack of beta glucouronidase activity. It is claimed that  Maconkey medium containing sorbitol, tellurite and cefixime


permit the growth of 94% of STEC and Shigella soniei but partially

or completely inhibit the growth of 67% of other strains

of E. coli [5,6].

Identification of STEC can be performed by identifying the

genes coding for verotoxins or by serology with increased serum

titer of specific antilipopolysaccharide antibodies [7,8].