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Verocytotoxin-producing Escherichia coli (VTEC) infections 

Verocytotoxin-producing Escherichia coli (VTEC) infections
Chapter:
Verocytotoxin-producing Escherichia coli (VTEC) infections
Author(s):

Mohamed A. Karmali

and Jan M. Sargeant

DOI:
10.1093/med/9780198570028.003.0008
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date: 28 September 2020

Verocytotoxin (VT)-producing Escherichia coli (VTEC), also known as Shiga toxin producing E. coli (STEC), are zoonotic agents, which cause a potentially fatal illness whose clinical spectrum includes diarrhoea, haemorrhagic colitis, and the haemolytic uraemic syndrome (HUS). VTEC are of serious public health concern because of their association with large outbreaks and with HUS, which is the leading cause of acute renal failure in children. Although over 200 different OH serotypes of VTEC have been associated with human illness, the vast majority of reported outbreaks and sporadic cases of VTEC-infection in humans have been associated with serotype O157:H7.

VTs constitute a family of related protein subunit exotoxins, the major ones implicated in human disease being VT1, VT2, and VT2c. Following their translocation into the circulation, VTs bind to endothelial cells of the renal glomeruli, and of other organs and tissues via a specific receptor globotriosylceramide (Gb 3), are internalized by a process of receptor-mediated endocytosis, and cause subcellular damage that results in the characteristic microangiopathic disease observed in HUS.

The incubation period of VTEC-associated illness is about 3–5 days. After ingestion VTEC (especially of serotype O157:H7) multiply in the bowel and colonize the mucosa of probably the large bowel with a characteristic attaching and effacing (AE) cytopathology. Colonization is followed by the translocation of VTs into the circulation and the subsequent manifestation of disease.

The majority of patients with uncomplicated VTEC infection recover fully with general supportive measures. Historically, the case-fatality rate was high for HUS. However, improvement in the treatment of renal failure and the attendant biochemical disturbances has substantially improved the outlook, although long-term sequelae may develop.

Ruminants, especially cattle, are the main reservoirs of VTEC. Infection is acquired through the ingestion of contaminated food, especially under-cooked hamburger, through direct contact with animals, via contaminated water or environments, or via personto-person transmission.

The occurrence of large outbreaks of food-borne VTEC-associated illness has promoted close scrutiny of this zoonoses at all levels in the chain of transmission, including the farm, abattoir, food processing, packaging and distribution plants, the wholesaler, the retailer and the consumer. While eradication of VTEC O157 at the farm may not be an option, interventions to increase animal resistance or to decrease animal exposure are being developed and validated. Hazard Analysis and Critical Control Programmes are being implemented in the processing sector and appear to be associated with temporal decreases in VTEC serotype O157 illness in humans. Education programmes targeting food handling procedures and hygiene practices are being advocated at the retail and consumer level. Continued efforts at all stages from the farm to the consumer will be necessary to reduce the risk of VTEC-associated illness in humans.

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