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.