Escherichia coli (E.coli) are very common bacteria in the gastrointestinal tract, and part of the normal bacterial flora. However, some E.coli strains are able to produce a toxin that could produce serious infection. The main reservoir of such E.coli strains is grass-feeding animals, cattle in particular. Their meat might become contaminated by faecal matter due to poor processing methods during slaughter, and their faeces might end up contaminating other foods (e.g. milk, vegetables) and water.
Humans acquire the infection by consuming contaminated food or water. Following an incubation period of about 3–4 days, a variety of gastrointestinal symptoms appear, ranging from mild to severe bloody diarrhoea, mostly without fever. However, about 8% of patients (children under five years old and the elderly being the most susceptible) may develop “haemolytic uraemic syndrome” (HUS), characterised by acute kidney failure, bleeding and neurological symptoms. Antibiotic therapy is not helpful (it might even favour HUS development). The death rate of HUS is about 3–5%.
Shiga toxin-producing E. coli (STEC)
Shiga toxin-producing E. coli (STEC) is a group of pathogenic Escherichia coli strains capable of producing Shiga toxins, with the potential to cause severe enteric and systemic disease in humans. The full serotype is usually defined by determining both O and H antigens. There are around 200 different E. coli O serotypes producing Shiga toxin, of which over 100 have been associated with human disease. Two major Shiga toxin types (Stx1 and Stx2) have been associated with strains causing human disease. While the serotype O157:H7 is considered as clinically the most important, it is estimated that up to 50% of STEC infections are caused by non-O157 serotypes. STEC is of public health concern because of the potential for outbreaks and the risk of serious complications. Haemolytic uremic syndrome (HUS) is considered as the most common cause of acute renal failure in European children. Even if the clinical presentation of non-O157 STEC infections may vary, they can be as virulent as O157:H7 infections.
Transmission of STEC infection mainly occurs through contaminated food or water and contact with animals. Person-to-person transmission is also possible among close contacts (families, childcare centres, nursing homes, etc). A wide variety of food has previously been implicated in outbreaks as suspected sources, including raw (unpasteurised) raw milk and cheese, undercooked beef, a variety of fresh produce (e.g. sprouts, spinach, lettuce), unpasteurised apple cider, etc. Recently an outbreak of STEC O157 infections in Canada and the USA was linked to walnuts, thus new sources continue to be identified. Various types of animals, in particular cattle and other ruminants, can be healthy carriers of human-pathogenic STEC that can be spread to humans through faecal contamination.
The infective dose is very low. The incubation period ranges from three to eight days. The typical
presentation of infections with STEC is acute gastroenteritis, often accompanied with mild fever and sometimes vomiting. The typically bloody diarrhoea is in most cases mild and self-limiting and most people recover within five to seven days. Around 15% of children diagnosed with STEC O157 infection develop the severe complication of HUS; this proportion is much lower among adults, and this proportion in outbreaks of non-O157 outbreaks is not well documented. The severity of STEC diarrhoea is determined by several factors, including the E. coli serotype, the type of Shiga toxin produced and other virulence characteristics of the bacteria. The patient’s age and the infecting dose also play an important role. Children under the age of 5 years are at higher risk of developing clinical disease when infected, and infants are at increased risk of death from dehydration and septicaemia.
While the confirmation methods of O157 STEC infection are well established, this is not always the case for infections caused by STEC non-O157 serotypes. Therefore, underreporting of non-O157 STEC infections is very likely, and their importance for clinical disease in humans is insufficiently understood.
The treatment of STEC infections is mainly based on rehydration, while antibiotic treatment is often contraindicated as it may activate Shiga toxin release and therefore cause clinical deterioration with a potential evolution to HUS.
STEC infections in humans are under epidemiological surveillance in the EU and in 2009 there were 3 573 reported cases of which about half were caused by the STEC O157:H7 serotype.
Since 2008, eight cases of STEC O104 have been reported in the EU, by Austria (one case in 2010), Belgium (two cases in 2008), Denmark (one case in 2008), Norway (three cases in 2009), and Sweden (one case in 2010); three of these cases were imported. In addition, between 2004 and 2009, Austria and Germany reported some positive findings of STEC O104 in food or animals. However, the suggested outbreak strain of serotype STEC 0104:H4 has been rarely reported worldwide.