The outbreak was a dramatic entrance to the world stage for the microbe at the center of it all, a little-known strain of E. coli known as O104:H4, that caused German authorities facing a nation of overwhelmed hospitals to declare on May 22, "Clearly, we are faced with an unusual situation."
O104 managed to wreak such an unprecedented level of devastation in Germany thanks to evolutionary adaptations that combined the defensive traits of some harmless strains with the deadly traits of Shiga toxin-producing strains such as O157:H7. While most toxic strains predominantly affect the young and old, O104 infected otherwise-healthy adults with debilitating illnesses that not only hospitalized a greater proportion, but lasted an average of two weeks instead of one.
Now, team led by researchers at Michigan State University has determined that those defensive traits O104 picked up from its ancestors just might become its greatest weakness. The new research, published in the current edition of the journal PLoS ONE, proposes a possible avenue for weakening the virulent strain and -- if all goes according to theory -- preventing it from causing severe illnesses like those witnessed in Germany.
According to the researchers, the key to O104's success is that unlike other toxic E. coli, it possesses an adaptation that allows multiple bacteria to group together and form a protective 'biofilm' to ward off its host's defenses.
If scientists could develop a way to disrupt this biofilm, they might be able to defend patients against serious O104 infections that might progress into kidney failure or even death.
"It does seem like it could be a possibility," said Shannon Manning, Ph.D., molecular biologist at MSU and co-author on the study. "Even if you wipe out the biofilm, you're still going to get the disease if the toxin is being produced, but it might not be as severe."
Manning told Food Safety News that her and colleagues have a few theories for how to disable the biofilm. One involves breeding mutant O104 strains genetically designed to fail at biofilm production.
Once in O104-infected humans, these mutant strains could reproduce in a way that genetically 'knocks out' O104's ability to produce the biofilm.
But even then, Manning said, researchers will need to consider how to deliver such a treatment to a population:
"Even if you do find the magical treatment, how do we figure out who to treat?" she asked. "Would we give it to people who are at risk? People who are already infected? It could be too late by the time symptoms appear."
The team conducted its research by testing O104 and O157 on sets of mice and observing the differences in how each strain affected its host. The O104-infected mice had approximately twice as long of an incubation period, with some receiving severe kidney lesions after up to two weeks.
Some O104-infected mice showed worse kidney lesions than others, suggesting to Manning that some O104 bacteria forms stronger biofilms than others, giving the team hope that they can grow mutant strains especially inept at creating the biofilm.
Manning said that she hoped her team's research could prove useful before O104 could cause another disaster like last year's outbreak in Germany. The rapid nature of microbiological evolution, however, almost guarantees that researchers will need to continue innovating as new strains surprise populations with unusual situation's reminiscent of Germany's.
"Of course we don't want these outbreaks to happen, but because of microbial evolution, it is likely that we will continue to see new strains emerge," Manning said. "Therefore, we are going to continue to come up with new ways to fight them and hopefully we can decrease the frequency of the life-threatening infections they can cause."
