title: Shiga toxin-producing Escherichia coli O104:H4: a new challenge for microbiology.
abstract: In 2011, Germany experienced the largest outbreak with a Shiga toxin-producing Escherichia coli (STEC) strain ever recorded. A series of environmental and trace-back and trace-forward investigations linked sprout consumption with the disease, but fecal-oral transmission was also documented. The genome sequences of the pathogen revealed a clonal outbreak with enteroaggregative E. coli (EAEC). Some EAEC virulence factors are carried on the virulence plasmid pAA. From an unknown source, the epidemic strains acquired a lambdoid prophage carrying the gene for the Shiga toxin. The resulting strains therefore possess two different mobile elements, a phage and a plasmid, contributing essential virulence genes. Shiga toxin is released by decaying bacteria in the gut, migrates through the intestinal barrier, and is transported via the blood to target organs, like the kidney. In a mouse model, probiotic bifidobacteria interfered with transport of the toxin through the gut mucosa. Researchers explored bacteriophages, bacteriocins, and low-molecular-weight inhibitors against STEC. Randomized controlled clinical trials of enterohemorrhagic E. coli (EHEC)-associated hemolytic uremic syndrome (HUS) patients found none of the interventions superior to supportive therapy alone. Antibodies against one subtype of Shiga toxin protected pigs against fatal neurological infection, while treatment with a toxin receptor decoy showed no effect in a clinical trial. Likewise, a monoclonal antibody directed against a complement protein led to mixed results. Plasma exchange and IgG immunoadsoprtion ameliorated the condition in small uncontrolled trials. The epidemic O104:H4 strains were resistant to all penicillins and cephalosporins but susceptible to carbapenems, which were recommended for treatment.
authors.affiliation: Department of Microbiology, University of Barcelona, Barcelona, Spain.
authors.forename: Maite
authors.initials: M
authors.lastname: Muniesa
authors.forename: Jens A
authors.initials: JA
authors.lastname: Hammerl
authors.forename: Stefan
authors.initials: S
authors.lastname: Hertwig
authors.forename: Bernd
authors.initials: B
authors.lastname: Appel
authors.forename: Harald
authors.initials: H
authors.lastname: Brüssow
mesh_terms: D000818:Animals; D000900:Anti-Bacterial Agents / Q000008:administration & dosage; D000907:Antibodies, Bacterial / Q000008:administration & dosage; D000992:Antitoxins / Q000008:administration & dosage; D001435:Bacteriophages / Q000235:genetics; D016000:Cluster Analysis; D004195:Disease Models, Animal; D004196:Disease Outbreaks; D004927:Escherichia coli Infections / Q000453:epidemiology* / Q000382:microbiology* / Q000473:pathology / Q000628:therapy; D005517:Foodborne Diseases / Q000453:epidemiology* / Q000382:microbiology* / Q000473:pathology / Q000628:therapy; D005858:Germany / Q000453:epidemiology; D006801:Humans; D007167:Immunotherapy / Q000379:methods; D051379:Mice; D017720:Molecular Epidemiology; D058889:Molecular Typing; D016032:Randomized Controlled Trials as Topic; D054323:Shiga-Toxigenic Escherichia coli / Q000145:classification / Q000235:genetics / Q000302:isolation & purification* / Q000472:pathogenicity*; D016896:Treatment Outcome
chemical_list: D000900:Anti-Bacterial Agents; D000907:Antibodies, Bacterial; D000992:Antitoxins