On June 10, officials of the German federal disease control center, the Robert Koch Institut, announced that raw vegetable sprouts were indeed the culprit in the outbreak that has sickened thousands of people and caused more than 30 deaths. They made the case using good old-fashioned shoe-leather epidemiology: a “recipe-based restaurant cohort study,” which found that people who ate sprouts were nearly nine times more likely to become infected than those who didn’t. Cucumbers, tomatoes, and lettuce—fingered early on as likely suspects—were all exonerated.
In an interview on National Public Radio’s All Things Considered news program, CDC Director Dr. Tom Frieden stated that the evidence implicating sprouts doesn’t constitute proof that they caused the outbreak. The “smoking gun,” he said, is DNA analysis proving that the bacteria isolated from sick people and the likely source are identical. Of the many environmental samples tested in the outbreak investigation so far, only one has yielded a match: an opened bag of sprouts in the garbage can at the home of two infected people. On the radio, Dr. Frieden confided that he gave up eating sprouts years ago, after becoming ill in India from sprouted seeds he had brought with him from the U.S.
DNA analysis of the implicated STEC quickly tipped off investigators to its bag of tricks. Science reported that German and Chinese scientists using new technology had sequenced the 5.2-million-base-pair genome in a matter of days and made the data available online for researchers to download. Within 24 hours, scientists from around the world had analyzed the genome data and identified some special features. Unlike the STECs commonly implicated in foodborne outbreaks, the current outbreak strain can form biofilms that help it cling to human intestines. It is also resistant to many antibiotics.
A striking aspect of the German outbreak is that approximately 1 in 4 infected persons developed hemolytic uremic syndrome (HUS). This life-threatening outcome of STEC infection is uncommon, developing in 5-10% of cases. So far, DNA analysis of the outbreak strain has not provided clues to explain these findings.
Every infection involves at least two genomes, one belonging to the pathogen and the other to its host. Studies of human genetics and HUS have focused mostly on a rare form of the disease that runs in families and is not associated with STEC infection. Recent research, however, suggests that most people who develop HUS—whether related to STEC infection or not—may have variants in genes associated with the clotting and complement pathways. To search the HuGE Navigator for references to scientific articles on human genetic variation in HUS, click here.
The Foodborne Diseases Active Surveillance Network (FoodNet) monitors more than 650 laboratories in 10 areas of the U.S. for illness caused by foodborne pathogens, including STEC, through an active collaboration of CDC, ten state and local health departments, the U.S. Department of Agriculture (USDA), and the Food and Drug Administration (FDA). FoodNet has incorporated human genetics into an epidemiologic study of risk factors for HUS in persons with STEC infection.
For more information about the recent outbreak in Germany, see: WHO Europe. Public health review of the enterohaemorrhagic Escherichia coli outbreak in Germany. June 10, 2011.