Peri- and Postharvest Factors in the Control of Shiga Toxin-Producing Escherichia coli in Beef

Abstract

Certain Shiga toxin-producing Escherichia coli (STEC) strains are important causes of food-borne disease, with hemorrhagic colitis and, in some cases, hemolytic-uremic syndrome as the clinical manifestations of illness. Six serogroups and one serotype of STEC (O26, O45, O103, O111, O121, O145, and O157:H7) are responsible for the vast majority of cases in the United States. Based on recent data for all food commodities combined, 55.3% and 50.0% of the outbreaks of STEC O157 and non-O157 in the United States, respectively, are attributable to beef as a food source. Consequently, the U.S. Department of Agriculture, Food Safety and Inspection Service declared these organisms as adulterants in raw, nonintact beef. In North America, cattle are a major reservoir of STEC strains, with organisms shed in the feces and contaminated hides of the animals being the main vehicle for spread to carcasses at slaughter. A number of peri- and postharvest interventions targeting STEC have been developed, and significant progress has been made in improving the microbiological quality of beef in the past 20 years as a result. However, continued improvements are needed, and accurate assessment of these interventions, especially for non-O157 STEC, would greatly benefit from improvements in detection methods for these organisms.

Valid Presumption of Shiga Toxin-Mediated Damage of Developing Erythrocytes in EHEC-Associated Hemolytic Uremic Syndrome

“…Cattle represent the most important source of human infections, where EHEC localize in the recto-anal junction of the animals [ 213 , 214 , 215 ]. EHEC O157 outbreaks are mostly linked to the consumption of contaminated bovine-derived products, including animal contact in petting zoos with lower incidence, as sources of STEC infections [ 211 , 213 , 216 , 217 , 218 , 219 ]. After ingestion, EHEC selectively colonize the mucosa of the human large intestine with the “attaching and effacing” mechanism, genetically governed by a large pathogenicity island defined as the Locus of Enterocyte Effacement (LEE) [ 211 , 220 , 221 , 222 , 223 , 224 , 225 ].…”

The effect of transportation and lairage on faecal shedding and carcass contamination withEscherichia coliO157 and O26 in very young calves in New Zealand

“…Ruminants, in particular cattle, have been identified as a major reservoir of Shiga toxin-producing Escherichia coli O157:H7 (STEC O157) and related non-O157 STEC serogroups (e.g. O26, O45, O103, O111, O121 and O145) [1], which are recognised as important zoonotic pathogens worldwide [2]. STEC can cause serious human illnesses such as haemorrhagic colitis and the potentially life-threatening haemolytic uraemic syndrome [3].…”

A Topographical Atlas of Shiga Toxin 2e Receptor Distribution in the Tissues of Weaned Piglets

“…In humans, subtypes Stx2a and Stx1a are the most prominent virulence factors of STEC isolates being responsible for severe gastrointestinal diseases and extraintestinal complications, including hemorrhagic colitis and hemolytic uremic syndrome (HUS) [6,7,8]. Cattle are the primary natural reservoir acting as symptomless carriers [9,10,11], although Stx is capable of exerting cytotoxic effects, e.g., on bovine lymphocytes [12,13,14]. In swine, Stx2e-producing STEC cause, typically during the first two weeks after weaning, the edema disease, an enterotoxemia characterized by subcutaneous, mesenteric and cerebral edemas with neurological impairment including ataxia, paralysis, and recumbency as main clinical signs [3].…”