It was the bean sprouts! The veggie-burger disease revisited.

By Siouxsie Wiles 17/06/2011 4


Finally the number of new cases from the German E. coli outbreak are easing. To date there have been 3362 people infected, with 823 people developing Haemolytic Uraemic Syndrome (HUS) and 37 deaths. Turns out the culprit was bean sprouts from an organic farm in lower Saxony. It does seem likely that the reason the majority of cases have been women in their 20’s to 40’s is that they are more likely to eat salads containing beansprouts, rather than it being due to some inherent features of the E. coli strain.

So what do we know about the bug? First a quick introduction to nasty E. coli strains. They are classified based on O and H proteins; O is the cell wall lipopolysaccharide (LPS) antigen and H the flagella antigen. There are also a number of different ‘classes’:

ETEC – enterotoxigenic E. coli cause diarrhoea without fever (bug produces enterotoxins)

EAEC – enteroaggregative E. coli cause watery diarrhoea without fever (bug produces a hemolysin and an enterotoxin)

EIEC – enteroinvasive E. coli cause profuse diarrhea and high fever

EPEC – enteropathogenic E. coli cause diarrhoea (bug does not produce enterotoxins, instead has a type III secretion system and uses a protein called intimin to bind to host intestinal cells)

EHEC – enterohaemorrhagic E.coli cause bloody diarrhoea and HUS (bug has type III secretion system and produces Shiga toxin) [may also be referred to as STEC -shiga-toxin producing E. coli]

As I wrote previously, the BGI (formally the Beijing Genomics Institute) sequenced the bacterium involved and released of the genomic data to the international community for ‘crowdsourcing’. And here is what the crowd have discovered:

1. The outbreak strain is serotype O104:H4, which has been reported to cause HUS before, in a young woman in Korea in 2006. This was unexpected, as the majority of E. coli outbreaks and HUS cases reported to date have been caused by EHEC O157:H7.

2. The outbreak strain appears to be an EAEC strain as it contains most of the adherence genes of typical EAEC and lacks intimin and the EPEC/EHEC type III secretion system.

3. Unlike normal EAEC the outbreak strain does not contain hemolysin.

4. Also unlike normal EAEC the outbreak strain has picked up a Shiga toxin (Stx2).

5. They are very antibiotic resistant, including possessing extended spectrum beta lactamases (ESBL’s) which confer resistance to cephalosporins.

Now the source has been identified, there will be a lots of questions asked as to how the bean sprouts became contaminated. Kat Holt has suggested that as EAEC strains have not been identified in animals, humans (most likely asymptomatic carriers) may be to blame. It may be that people handling food need to be screened to make sure they are not carriers. Whatever happens though, it is clear that new regulations and improved surveillance and disease prevention strategies are needed to stop such an outbreak occurring again.


4 Responses to “It was the bean sprouts! The veggie-burger disease revisited.”

  • Thanks for this – interesting. For those who are interested, HUS causes Acute Kidney Injury (previously known as Acute Renal Failure) which is likely cause of death. AKI is my area of research and the biggest issue is that there are no effective treatment apart from dialysis (which is really late in the game and is associated with a 50% mortality rate). The #1 reason for there being no effective treatment is because AKI is not easily detected. AKI is simply the filtration function of the kidney partially shutting down. Current detection is by a plasma marker that gradually builds up until it is noticeable a couple of days after the event (think of a partially blocked drain that takes a couple of days before it overflows).
    The good news is that in the last decade numerous new biomarkers have been detected which seem to pick up on the injury itself early on in the peace. To show off a little (surely NZ scientists are allowed to on Sciblogs) we (in Chch & Dn) recently ran the world’s first randomised control trial of a novel intervention using one of these injury biomarkers to triage (see Endre ZH, Walker RJ, Pickering JW, Shaw GM, Frampton CM, Henderson SJ, et al. Early intervention with erythropoietin does not affect the outcome of acute kidney injury (the EARLYARF trial). Kidney Int. 2010 Jun.;77(11):1020–1030.