The continuing evolution of E. coli O157:H7

Escherichia coli First recognized a quarter of a century ago, E. coli O157:H7 causes bloody and non-bloody diarrhoea, 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 of secreted effector proteins encoded in the LEE and elsewhere in the genome.

The work of Manning et al (Variation in virulence among clades of Escherichia coli O157:H7 associated with disease outbreaks. 2008 PNAS USA 105:4868–4873) reminds us that evolution of microbial agents is an ongoing process. E. coli O157:H7 is the most notorious of several different types of pathogenic E. coli that are “relentlessly evolving” (7). This study demonstrates the power of current molecular techniques, where the entire genome sequence of a bacterial pathogen can be determined to investigate a specific disease outbreak, but it also demonstrates the limitations of such techniques in relating the sequence information to the complex interaction of host and pathogen.

The continuing evolution of a bacterial pathogen
PNAS Early Edition, March 19, 2008

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One Comment

  • ecoli says:

    microbe evolution never ceases to fascinate me. The short generation time of E. coli, plus tremendous selection for the immune system causes systems to change really quickly. I wrote up something a but similar about uropathogenic E. coli strains, in my own blog.