Researchers from Michigan State University have decoded the E.coli strain that led to more than 50 deaths last year.
Shannon Manning et al found increased production of the Shiga toxin was the probable culprit as it has a longer incubation period than other E.coli strains.
The outbreak of E.coli O104:H4 killed 54 and sickened 4,000 and was centred in northern Germany but affected 15 other countries in Europe and North America.
After looking at the bacteria's biofilm, the grouping of E.coli bacteria that stick to surfaces and grow in a self-produced protective coat, the researchers were able to determine that the bacterium makes more Shiga toxin.
Increased production of Shiga toxin is the likely cause of so many incidents of kidney damage and death during the 2011 outbreak, said the researchers.
They found the incubation period was longer among individuals infected with O104:H4 compared with O157:H7 because it needs more time to form a biofilm, which is not critical for O157 infections.
“Our data suggests that the O104:H4 strain expresses genes important for biofilm formation during in vivo infection but that O157:H7 does not,” said the researchers in the academic journal PloS ONE.
The scientists, led by Shannon Manning from Michigan State University’s microbiology and molecular genetics department, found the incubation period was longer than the 0157 strain of E.coli.
She told FoodProductionDaily.com: “We had a case in Michigan of someone who had travelled to Germany and eaten the contaminated sprouts so we got the strain from Michigan Health Department and put it into the mice.
“For seven days they were fine so we waited for 14 days and while the mice weren’t dead they did have kidney legions.
“The variation across mice was seen in the outbreak in humans, some had diarrhoea and in others it led to kidney failure and death.”
Manning said the strain is different in producing biofilm in each host, which affects the level of toxins.
“It has a longer incubation period than O157 and it takes longer to colonize the host and form the biofilm.”
The next phase of Manning's research will focus on creating mutant strains in an effort to prevent the bacterium from forming a biofilm.
This would stop the disease as conditions would not be favourable for bacterial growth.
“With clues how the strain is behaving inside the host we can use different preventive strategies to prevent the formation of the biofilm.
“We know strains evolve and while we can’t predict when and how it will happen we can be prepared to tackle the strains and prevent or decrease them when you know what you are dealing with.”
Source: PLoS ONE
Published online ahead of print, doi: 10.1371/journal.pone.0041628
“Correlation between In Vivo Biofilm Formation and Virulence Gene Expression in Escherichia coli O104:H4”
Authors: Rim Al Safadi, Galeb S. Abu-Ali, Rudolph E. Sloup, James T. Rudrik, Christopher M. Waters, Kathryn A. Eaton, Shannon D. Manning