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Deadly E. coli strain decoded

By R&D Editors | July 26, 2012

The secret to the deadly 2011 Escherichia coli (E. coli) outbreak in Germany has been decoded, thanks to
research conducted at Michigan State University (MSU).

The deadliest E. coli outbreak ever, which caused 54 deaths and sickened more than
3,800 people, was traced to a particularly virulent strain that researchers had
never seen in an outbreak before. In PLoS
ONE
, a team of researchers led by Shannon Manning, MSU molecular biologist
and epidemiologist, suggests a way to potentially tame the killer bacteria.

The strain, E. coli O104:H4, shares some characteristics as other deadly E. coli bacteria, but its combination is
novel. Researchers haven’t determined the mechanism it uses to cause disease, although
Manning and her team were able to find the strain’s Achilles heel—its biofilm.

By focusing on the bacteria’s biofilm, the
grouping of many E. coli bacteria
that stick to a cell’s surface and grow encased in a self-produced protective
coat, Manning and colleagues were able to determine why it was so deadly. When
the bacterium found in Germany forms a biofilm, it begins to make more toxic
genes like the Shiga toxin.

Increased production of the Shiga toxin is
the probable culprit that contributed to so many incidents of kidney damage and
death during the 2011 outbreak, Manning said.

“What made the German outbreak so different
is that many victims suffering from kidney failure were adults,” she said. “Rather than attacking adults, other types of E. coli that produce Shiga toxins typically damage kidneys of
children under 10.”

In addition, the incubation period was
considerably longer among individuals infected with the German outbreak strain
compared to individuals infected with E.
coli
O157, a similar bacterium that can also cause illness and death.
Manning believes this is because the German strain needs a longer period of
time to form a biofilm, whereas biofilms are not important for O157 infections.

“Our research demonstrates that biofilm
formation is critical for toxin production and kidney damage,” she said. “If we
can block the bacteria from forming a stable biofilm, then it is likely that we
can prevent future E. coli O104:H4
infections.”

The next phase of Manning’s research is
already focusing on creating mutant strains in an effort to prevent the
bacterium from forming a biofilm. This would prevent the disease completely
since the conditions would not be favorable for bacterial growth.

Source: Michigan State University

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