Escherichia coli is a bacterium that is commonly found in the lower intestine of animals. Nonpathogenic, intestinal Escherichia coli (commensal E. coli) support the physiological intestinal balance of the host, whereas pathogenic E. coli with typical virulence factor gene profiles can cause severe outbreaks of different diseases (e.g. Edema (Oedema) Disease, diarrhea).
Edema (Oedema) Disease is caused by Shigatoxin (Stx2e). This toxin is produced by a specific virotype of Escherichia coli - which is named STEC (graphic). A virotype is determined by a particular combination of virulence genes. Important virulence factors encoded by EDEC are the fimbrial adhesin F18 and Shigatoxin (Stx2e).
While the E. coli encoding for Shigatoxin (Stx2e) occur worldwide, prevalence data particularly from healthy herds are rarely available. Nevertheless, a recently published longitudinal study in three US farms with healthy pigs observed a high prevalence (68.3%) of Shigatoxin-encoding Escherichia coli (STEC) in pigs raised for pork production. The usual detection rate of Stx2e in cases with clinical signs suspicious for ED is around 20% up to 60%.
Shigatoxins (Stx) are a family of related toxins with two major groups, Stx1 and Stx2. The toxins are named for Kiyoshi Shiga, who first described the bacterial origin of dysentery caused by Shigella dysenteriae. The most common sources for Shigatoxin are the bacteria S. dysenteriae and the shigatoxinogenic virotypes of Escherichia coli (STEC), and other enterohemorrhagic E. coli (EHEC).
The toxins are named for Kiyoshi Shiga, who first described the bacterial origin of dysentery caused by Shigella dysenteriae. The most common sources for Shigatoxin are the bacteria S. dysenteriae and the shigatoxigenic serotypes of Escherichia coli (STEC), and other enterohemorrhagic E. coli (EHEC).
Shiga-like toxins 1 and 2 are the Shigatoxins produced by some E. coli strains. Stx-1 is identical to Stx (true Shiga toxin – is produced by Shigella dysenteriae) or differs by only one amino acid. Stx-2 shares 56% sequence identity with Stx-1.
The name verocytotoxins/verotoxins – a seldom-used term for Stx – is from the hypersensitivity of the so-called Vero cells (used in cell cultures) to Stx. The toxin has two subunits—designated A and B (graphic). The B subunit is a pentamer that binds to specific glycolipids on the host cell. Following this, the A subunit is internalized and cleaved into two parts. The A1 component then binds to the ribosome, disrupting the protein synthesis. Stx-2 has been found to be about 400 times more toxic (as quantified by LD50 in mice) than Stx-1.
(Source: Sato et al. 2013 J. Vet. Med. Sci.; Tu et al. 2009 Protein Expression and Purification)
The mainly affected production stages are recently weaned pigs, pigs during nursery and younger finishing pigs.
F18 is one of the well known adhesion factors, which enables E. coli the attachment to the intestinal mucosa. Stx2e encoding strains may possess either the fimbrial variant F18ab or F18ac.
Susceptibility to colonization and to infection with an E. coli F18 strain develops around weaning and is dependent on the presence of the porcine intestinal F18 receptor (F18R) genotype.
The expression of F18R is age-dependent and begins at around three weeks of age.
Torrison at al. (graphic) described the main stages of pigs life where E. coli encoding for Stx2e are detected with a peak in the weeks seven to nine. This corresponds with the experience of Ceva in many countries worldwide.
Remarkably Stx2e can be detected also in later production stages . If so, it is generally the origin of serious clinical signs, increased mortality and impaired performance.
Yet F18 is not detectable in every case of E. coli encoding for Stx2e (up to 20%). The relevance of these particular E. coli (without the F18 but with Stx2e) is nevertheless given, as they have been isolated as only pathogen from cases with severe clinical signs.