A previously healthy 11 year old girl develops a gastrointestinal infection with cramping and watery stools. After several days, she begins to pass blood per rectum, and is hospitalized for dehydration. In the hospital, she is noted to have decreasing urine output with rising blood urea nitrogen (BUN). Total blood count reveals anemia and thrombocytopenia, and the peripheral smear is remarkable for fragmented red cells (schistocytes). Infection with which of the following bacterial genera is most likely responsible for this syndrome?

This patient has developed hemolytic-uremic syndrome (HUS), a complication of the Shiga toxin or Shiga-like toxin: exotoxins released by Shigella species and the enterohemorrhagic E.coli. HUS in children usually develops after a gastrointestinal or flu-like illness, and is characterized by bleeding, oliguria, hematuria and microangiopathic hemolytic anemia. Presumably the Shiga toxin is toxic to the microvasculature, producing microthrombi that consume platelets and RBCs, and may fragment the red cell membrane. The incorrect choices are all bacteria which may produce an enterocolitis, but do not elicit HUS. A long-term consequence of Campylobacter infection is a reactive ahritis or full-blown Reiter's syndrome. Clostridial enterocolitis is produced by Clostridium difficile, a normal inhabitant of the gut that produces pseudomembranous colitis when other gut flora are suppressed by treatment with antibiotics. Typhoid fever (produced by Salmonella typhi and S. paratyphi) produces a protracted illness that progresses over several weeks and includes rash and very high fevers, but not HUS. Ref: Ray C.G., Ryan K.J. (2010). Chapter 33. Enterobacteriaceae. In C.G. Ray, K.J. Ryan (Eds), Sherris Medical Microbiology, 5e.