The continuing evolution of a bacterial pathogen

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Abstract
Although Escherichia coli is a prototypic commensal bacterial species of the mammalian intestine and a laboratory workhorse for molecular biology, certain strains of this species are capable of causing significant human disease. The spectrum of disease caused by E. coli includes enteric/diarrheal disease, urinary tract infections, renal failure, and sepsis/meningitis (1). The different pathotypes of E. coli possess genes encoding a wide variety of virulence factors that are frequently encoded on mobile genetic elements such as bacteriophages, plasmids, and pathogenicity islands. E. coli strains can be serotyped as one of >10,000 possible combinations of O (LPS) and H (flagellar) antigens, but one serotype, O157:H7, has achieved particular notoriety as a cause of deadly outbreaks of food-borne illness throughout the world. The work of Manning et al. (2) in this issue of PNAS reveals significant new information on the evolution and genetic composition of E. coli strains belonging to the O157:H7 serotype and reports the emergence of a new variant that appears to cause more severe disease. First recognized a quarter of a century ago, E. coli O157:H7 causes bloody and nonbloody diarrhea, hemorrhagic colitis, and hemolytic uremic syndrome (HUS), which is the leading cause of acute renal failure in children. One of the most potent toxins ever described, Shiga toxin, is a critical virulence factor in HUS, and different variants of this bacteriophage-encoded toxin, e.g., Stx1, Stx2, Stx2c, are found in this pathogen. The mechanism of Shiga toxin is similar to that of ricin and involves inhibition of protein synthesis in renal endothelial and other cells. Toxin produced in the intestine enters the circulation, resulting in direct and indirect effects on the kidney. Other important virulence factors include the type III secretion system encoded on the locus of enterocyte effacement (LEE) pathogenicity island and a variety …