Washington: Researchers have decoded the deadly 2011 E. coli outbreak in Germany, which killed 54 people and sickened more than 3,800, tracing it to a particularly virulent strain.
A team led by Shannon Manning, molecular biologist and epidemiologist at the Michigan state University, suggests a way to potentially tame the killer bug, named as E. coli O104:H4, shares some characteristics as other deadly E. coli bacteria, but its combination is novel.
They haven`t yet figured out the mechanism it uses to trigger disease, although Manning and her team were able to find the strain`s Achilles heel - its bio-film, the journal Public Library of Science ONE reported.
By focusing on the bug`s bio-film, 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 bio-film, 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, according to a university statement.
"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."
Besides, the incubation period was considerably longer among individuals infected with the German outbreak strain compared to individuals infected with E. coli O157, a similar bug that can also cause illness and death.
Manning believes this is because the German strain needs a longer period of time to form a bio-film, whereas bio-films are not important for O157 infections.
"Our research demonstrates that bio-film formation is critical for toxin production and kidney damage," she said. "If we can block the bacteria from forming a stable bio-film, then it is likely that we can prevent future E. coli O104:H4 infections."
Chris Waters, assistant professor of microbiology and molecular genetics at Michigan and colleagues co-authored the study.