German officials declare E. coli O104:H4 a sproutbreak

Via H5N1, German officials are calling it for sprouts:

Germany on Friday blamed sprouts for a bacteria outbreak that has left at least 30 dead and some 3,000 ill, and cost farmers across Europe hundreds of millions in lost sales.

“It’s the sprouts,” Reinhard Burger, the president of the Robert Koch Institute, Germany’s national disease centre, told a news conference on the outbreak of enterohaemorrhagic E. coli (EHEC) in northern Germany.

“People who ate sprouts were found to be nine times more likely to have bloody diarrhoea or other signs of EHEC infection than those who did not,” he said, citing a study of more than 100 people who fell ill after dining in restaurants.

As a result, the government lifted a warning against eating raw tomatoes, lettuce and cucumbers.

There still haven’t been any positive tests, but as I mentioned yesterday, the epi seems to strongly point to sprouts. Confirmation via bacterial isolation and typing would be ideal, but I’m not holding my breath for that to happen at this late date. Larger studies also, I’m hoping, will be done–the numbers above state that they came from ~100 people, out of approximately 3,000 sickened so far, and we still don’t know how the implicated sprouts were contaminated. Did it originate in the seeds? (If so, still from where?) Was it human-to-sprout contamination from a sick worker on the farm? (If so, where again did the worker pick it up?) Still so many unanswered questions, but at least this should let some of the other farmers’ lives get back on track.

The case of the missing smoking sprouts

Maryn McKenna has a great update today on the E. coli situation, looking at where we are as far as unanswered questions about the outbreak and the strain. It’s been a messy day; more evidence seems to point to the sprout farm, but CIDRAP also notes that another contaminated cucumber was found in the compost bin of a family sickened by the bacterium (this one had the correct serotype–O104), but it’s impossible to tell at this point whether the cucumber was the source of that bacterium or it ended up there from one of the sickened family members. Twists and turns abound in this investigation. I’ve not seen any confirmation that the remaining sprout isolates tested negative yet, either.

One thing I want to emphasize and expand upon, from the CIDRAP article:

Most of the investigation findings point back to a sprout source, and microbiological testing a month after the fact doesn’t change that, Hedberg said. “Negative micro results cannot negate positive epi results. This is an important principle that we cannot state too strongly.”

At this late date, it’s hard to say whether we’ll be able to definitively trace this back to its source–too much time may have passed for there to be any remaining contaminated source material left. This means we might not ever find the “smoking gun” (or smoking sprouts, as the case may be). With such a severe outbreak–725 cases of hemolytic uremic syndrome, over a quarter of those infected–that’s bad news if we can’t confirm the vehicle, as it may make it more difficult to find the ultimate source of this strain. However, as Hedberg notes, we do still have the epi. This was used long before we had today’s molecular typing techniques, or even before we had microbiology culture ability, for that matter. Think John Snow’s cholera investigations, where he didn’t even know about bacteria and yet was able to determine the water as the vehicle for infection. So while confirmation may not happen, it’s still looking like most lines of evidence point to the implicated farm.

Maryn also brings up a great point that what we’re seeing as far as cases may be over-estimating the actual severity of the infection. I’ve talked about this previously regarding influenza infections, particularly H5N1. Right now H5N1 has a high mortality rate–but is it artificially high, because mild or asymptomatic infections are being missed?

With O104, as with any food-borne infection, surely this is happening. Mild diarrhea or stomach cramping isn’t something people frequently go to their healthcare provider over, so inevitably cases are missed. However, it probably happens with any E. coli outbreak, yet in most others we still see HUS rates between about 2-7% of the confirmed infections, while this one is at about 26%. So it doesn’t seem (to me, at least) that missed mild infections are the whole story. Is this acting like the novel Clostridium difficile strains, which have a mutation in a regulatory gene that leads them to pump out higher levels of toxin than “regular” strains? More than just genetic analysis will be needed to investigate that–some basic microbiology will also be needed. If nothing else, this outbreak has given us much research fodder over the coming years.

E. coli update: sprouts as the culprit?

The E. coli story is moving quickly. A news report out today suggests that sprouts might be the culprit (though it should be emphasized that the outbreak strain hasn’t been isolated from these vegetables yet):

Mr Lindemann said epidemiological studies all seemed to point to the plant nursery in Uelzen in the state of Lower Saxony, about 100km (62m) south of Hamburg – though official tests had not yet shown the presence of the bacteria there.

“Further evidence has emerged which points to a plant nursery in Uelzen as the source of the EHEC cases, or at least one of the sources,” he said.

“The nursery grows a wide variety of beansprouts from seeds imported from different countries.”

As far as the molecular analyses, Kat Holt and David Holme have been doing some additional analyses of the released genome sequences, and it looks like this is an old strain of enteroaggregative E. coli (the type which usually cause more run-of-the-mill diarrhea; free review here, but it’s a bit dated) which has simply acquired the Shiga toxin. From Kat:

It will be interesting to see what more can be found as the assemblies of the strains are improved with additional data. While the analysis so far suggests that this is a classic case of E. coli sharing genes via various mechanisms of horizontal transfer (i.e. bacteria doing what bacteria do), it will be very interesting to tease out the subtleties of the virulence genes and how they interplay to result in this particularly virulent bug.

For me, another interesting unanswered question will be the origin–if it’s on the sprouts, how did it get there? Are animals in the area carrying this? Why so many antibiotic resistance genes? Still quite a bit to learn, even if the sprouts indeed turn out to be the vehicle.