DNA sequencing is available to map the genome of E. coli O104:H4 within days
In May 2011, a virtually unknown strain of E. coli, known as E. coli O104:H4, made worldwide headlines when an outbreak in Germany sickened approximately 4,000 people and killed 50, including one American. This event, linked to fresh sprouts, quickly became the deadliest foodborne illness outbreak in history.
In the days following the first reports of illness,
microbiological research laboratories around the globe began pooling resources
to coordinate the world’s first “open source” analysis of a microbial genome.
In turn, this spurred an unprecedented level of focused study by international collaborators
that are still going on two years later.
Before the German outbreak, the only reported illness
associated with E coli O104:H4 was in
South Korea and involved a solitary case of hemolytic uremic syndrome, or HUS,
a potentially fatal kidney disease associated with severe E. coli infections.
Little to no research had focused on the rare strain
leading up to its record-setting outbreak. But, as soon as it hit, E. coli O104:H4 rose in notoriety to a
status reserved for E. coli O157:H7,
the strain that has caused numerous deadly outbreaks in the past two decades
and made E. coli a household name.
Thanks to recent technological advancements in DNA
sequencing, researchers around the world were able to map the genome of E. coli O104:H4 within days – a feat
that would have taken months if the outbreak had happened a decade earlier.
The combination of virulence traits could also explain
why the German outbreak saw such a high proportion of HUS cases. Nearly 1,000
of the 4,000 ill – or one in four – developed HUS as part of their infection.
Outbreaks of other E. coli strains
typically result in about one in 10 patients developing HUS, predominantly
children. What’s more, the E. coli O104:H4
outbreak caused HUS in adults at the same rate it did in children.
The use of antibiotics against Shiga toxin-producing E. coli has a well-established link with
higher rates of HUS due to bacteria releasing additional toxin when killed. In
July 2012, research from the University of New Mexico Children’s Hospital found
that treating children’s E. coli
infections with antibiotics tripled
their risk of developing HUS.
A team out of Michigan State University has been
experimenting with those gene transfers in an attempt to transfer anti-biofilm
genes back to O104:H4.In theory, any common anti-biofilm compound might be
useful for weakening. E coli O104:H4
enough for immune systems to better defend against it.
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