Verotoxin-Producing Escherichia coli in Spain: Prevalence, Serotypes, and Virulence Genes of O157:H7 and Non-O157 VTEC in Ruminants, Raw Beef Products, and Humans

Abstract

In Spain, as in many other countries, verotoxin-producing Escherichia coli (VTEC) strains have been frequently isolated from cattle, sheep, and foods. VTEC strains have caused seven outbreaks in Spain (six caused by E. coli O157:H7 and one by E. coli O111:H- [nonmotile]) in recent years. An analysis of the serotypes indicated serological diversity. Among the strains isolated from humans, serotypes O26:H11, O111:H-, and O157:H7 were found to be more prevalent. The most frequently detected serotypes in cattle were O20:H19, O22:H8, O26:H11, O77:H41, O105:H18, O113:H21, O157:H7, O171:H2, and OUT (O untypeable):H19. Different VTEC serotypes (e.g., O5:H-, O6:H10, O91:H-, O117:H-, O128:H-, O128:H2, O146:H8, O146:H21, O156:H-, and OUT:H21) were found more frequently in sheep. These observations suggest a host serotype specificity for some VTEC. Numerous bovine and ovine VTEC serotypes detected in Spain were associated with human illnesses, confirming that ruminants are important reservoirs of pathogenic VTEC. VTEC can produce one or two toxins (VT1 and VT2) that cause human illnesses. These toxins are different proteins encoded by different genes. Another virulence factor expressed by VTEC is the protein intimin that is responsible for intimate attachment of VTEC and effacing lesions in the intestinal mucosa. This virulence factor is encoded by the chromosomal gene eae. The eae gene was found at a much less frequency in bovine (17%) and ovine (5%) than in human (45%) non-O157 VTEC strains. This may support the evidence that the eae gene contributes significantly to the virulence of human VTEC strains and that many animal non-O157 VTEC strains are less pathogenic to humans.

Distribution of serotypes and virulence-associated genes in pathogenicEscherichia coliisolated from ducks

“…Haemorrhagic colitis and haemolytic-uraemic syndromes had a close association with non-O157 STEC serogroups such as O26, O91 and O78, causing a threat to human health (Seto et al, 2007). The serogroups of STEC identified in the present study were shown to be O36, O60, O77, O78, O158 and O78&O92, among which O77 had been detected in STEC of cattle and sheep (Blanco et al, 2003), and STEC O78 had been found in humans, sheep, pigs and birds, and it was also the predominant serogroup of APEC (Fratamico et al, 2004;Shaheen et al, 2004). O158 has also been found in STEC strains isolated from cattle and sheep (Fratamico et al, 2004;Wenz et al, 2006).…”

Molecular Characterization of Escherichia coli O157:H7 and non-O157 Shiga Toxin Producing E. coli from Retail Meat and Humans

“…E. coli O157:H7 has been widely known to be directly linked with foodborne infections, however, outbreaks due to non-O157 E. coli have increased recently [4]. Other serogroups including E. coli O26, O91, O103, O111, O118, O113and O145 have been reported as STEC [5][6][7]. Many STEC harbor shiga toxin 1 and shiga toxin 2 genes (stx1and stx2), such genes are responsible for the damage of endothelial and tubular cells resulting in acute renal failure [8].…”

Veterinary Public Health Approach to Managing Pathogenic Verocytotoxigenic Escherichia coli in the Agri-Food Chain

“…Shedding of VTEC by cattle is generally intermittent, with herd members remaining negative for months, with only a proportion sporadically becoming positive for a few weeks at a time (30,31). Carriage rates are higher in calves than in adult cattle, and while detected all year-round, carriage rates are subject to seasonal effects, with higher rates reported in spring and summer.…”