Scientists at Michigan State University in East Lansing have uncovered a key factor in the virulence of the genome of E. coli 0104:H4, the rare strain behind the outbreak in Germany last summer that killed 54 people and sickened nearly 4,000.
Their genome sequencing data demonstrated that the strain—one that had never before been linked to an outbreak of foodborne illness—is an enteroaggregative variety of E. coli. Like other enteroaggregative strains, 0104:H4 forms a biofilm, a grouping of many E. coli bacteria that stick to a cell’s surface and grow encased in a self-produced protective coat. But, unlike those varieties, 0104:H4 also has the ability to produce the Shiga toxin that can cause kidney failure and death, explained Shannon Manning, PhD, the assistant professor of molecular biology and epidemiology who led the research.
The E. coli strain most commonly associated with illness and hospitalization, 0157:H7, also forms a biofilm; in that strain, however, the biofilm is not important to its ability to cause infection. When 0104:H4 forms a biofilm, it begins to make more toxic genes like the Shiga toxin.
“The outbreak strain’s biofilm was over seven times thicker than O157’s biofilm in vitro,” said Dr. Manning. “Additionally, the outbreak strain overexpressed genes encoding the exopolysaccharide, the self-produced substance that encases the bacterial cells living within a biofilm, whereas O157 did not.”
The increased Shiga toxin production associated with the biofilm was likely the contributing factor that led to so many illnesses and deaths in the German outbreak, which suggests a therapeutic target. “It’s possible that therapeutics could be administered to people to prevent the bacteria from forming a biofilm altogether,” Dr. Manning said, noting that this is a project she is already working on. “Some antibiofilm agents have previously been tested on biofilm-based bacterial infections such as Staphylococcus and Pseudomonas.”
The research appears in the July 25 edition of the online journal PLoS ONE.