Escherichia coli are Gram-negative rod-shaped bacteria and part of the normal bacterial flora in the gastrointestinal tract, while diarrhoeagenic E. colipathotypes such as Shiga toxin-producing E. coli (STEC) and enteropathogenic E. coli (EPEC) are able to cause gastrointestinal infections [1]. STEC can lead to a severe disease, such as haemolytic-uraemic syndrome (HUS) [2]. The risk of HUS has been related especially to children under 5 years and to elderly people. HUS is characterised by acute onset of microangiopathic haemolytic anaemia, renal injury and low platelet count.
More than 400 STEC serotypes have been recognised, of which the best-known serotype is O157:H7 [1]. The most common non-O157:H7 serotypes causing human infections are O26, O103, O111 and O145 [3]. The virulence of STEC is largely based on the production of Shiga toxin 1 or 2 and is identified by detecting the presence of stx1 or stx2 genes [1,4]. The virulence of EPEC is caused by its capability to form attaching and effacing (A/E) lesions in the small intestine. This capability requires the presence of virulence genes called the locus of enterocyte effacement (LEE) in a pathogenity island (PAI) that encodes intimin [4]. Unlike STEC, EPEC do not produce Shiga toxin. EPEC are divided into two distinct groups by the presence of EPEC adherence factor plasmid (pEAF) expressing bundle-forming pili (BFP), which is a virulence determinant of typical EPEC (tEPEC) [5]. Thus atypical EPEC (aEPEC) are defined as E. coli that produce A/E lesions but do not express BFP. Typical EPEC are best known as a cause of infantile diarrhoea, especially in developing countries [6]. Diarrhoea-causing aEPEC have been shown to be separate group without a close relation to tEPEC, but some serotypes are genetically related to STEC [5]. The pathogenity of aEPEC has been questioned but their involvement with diarrhoeal outbreaks supports the idea that certain strains are diarrhoeagenic [1,7].
Both STEC and EPEC are transmitted through the faecal-oral route, and outbreaks caused by STEC and aEPEC have been described after ingestion of contaminated food or water [7,8]. STEC is common in ruminants and can be found in foods contaminated by ruminant faeces [9]. Most studies on STEC have focused on the serotype O157:H7, but infections and outbreaks caused by non-O157 strains are increasingly reported in Europe and elsewhere [10–13]. Atypical EPEC strains are found in animals used for food production, such as cattle, sheep, goat, pig and poultry, in contrast to tEPEC that has been found only in humans [1,14].
Since 1995, clinicians and clinical microbiology laboratories have been obliged to report culture-confirmed STEC infections to the Finnish Infectious Disease Registry (FIDR) maintained by the National Institute for Health and Welfare (THL) in Finland. EPEC infections are not reportable. Since PCR instead of culture became the standard for screening of diarrhoeal patients in 2013, the incidence of reported STEC infections has increased in Finland to 1.2–1.8 per 100,000 population between 2013 and 2015 compared with 0.2–0.6 per 100,000 between 2000 and 2012. From 1997 to 2015, six food- or waterborne STEC outbreaks were detected in Finland (Table 1).
Outbreak of multiple strains of non-O157 Shiga toxin-producing and enteropathogenic Escherichia coli associated with rocket salad, Finland, autumn 2016
15.may.18
Eurosurvelliance, Volume 23, Issue 35, https://doi.org/10.2807/1560-7917.ES.2018.23.35.1700666
Sohvi Kinnula, Kaisa Hemminki, Hannele Kotilainen, Eeva Ruotsalainen, Eveliina Tarkka,Saara Salmenlinna, Saija Hallanvuo, Elina Leinonen, Ollgren Jukka, Ruska Rimhanen-Finne
https://www.eurosurveillance.org/content/10.2807/1560-7917.ES.2018.23.35.170066