Aspects Of Microbial Evolution

One of the foremost examples of microbial evolution and its impact on society involves E. coli O157:H7. E. is a member of the family Enterobacteriaceae. Molecular phylogeny studies indicate that it is closely related to other mammalian pathogens such as Vibrio, Shigella, Salmonella, and Haemophilus (27). The enterobacteria are facultative anaerobes, allowing them to live anaereobically as commensulate organisms inside the mammalian intestine and aerobically in various terrestrial environments. Horizontal or lateral gene transfer via sexual recombination, transduction (phage infection), and transformation (direct uptake of naked DNA) is known to occur with strains of E. coli. Escherichia coli O157:H7 is an exceptionally lethal example of a harmless commensulate organism (non-pathogenic E. coli) that has sequentially acquired a number of discreet genes, each of which enhances human pathogenicity.

O157:H7 strains of E. coli are usually described as enterohemolytic, frequently causing hemolytic-uremic syndrome (HUS) with an unusually low infectious dose estimated to be below 100 CFU (28) and a notably high fatality of 10% for those developing HUS (29). Prior to 1982, outbreaks of hemorrhagic colitis and HUS were not reported as attributable to the O157:H7 serotype, this implies that it is a newly emerged pathogen and serotype.

There are presently four recognized phenotypic properties that characterize O157:H7 strains of E. coli: (1) inability to ferment sorbitol within 24 hrs, (2) inability to produce P-glucuronidase, (3) poor growth above 44°C, and (4) significantly greater acid tolerance than commensurate strains of E. coli. In addition, most strains of E. coli O157:H7 produce the shiga-like toxins SLT1 and SLT2, which are encoded for by two independent temperate phages that have presumably previously passed through a strain of Shigella shiga with incorporation of the toxin DNA sequences into their genomic DNA, and also harbor a large enterocyte attachment factor (EAF) 60-Mdalt plasmid, designated pO157, that encodes several genes involved in pilus formation and attachment to enterocytes and hemolysin production. The remaining known genes (at least 7) involved in pathogenicity are located in a 35.6 kb chromosomal pathogenicity island termed the locus of enterocyte effacement (30,31,32). The presence of plasmids is known to be associated with the acquisition of virulence factors and antibiotic resistance. In addition, the hypermutable state of O157:H7 strains presumably confers even greater genetic diversity than is present with commensurate strains (33). Inferential conclusions from experimental data indicate that strains of E. coli derived from humans are subject to significant levels of gene transfer and genetic recombination (27). Clonal analysis suggests that the immediate ancestor of O157:H7 was a pathogenic clone with a propensity to acquire new virulence factors in nature (34,35). The evolutionary sequence presumably involved has been elegantly presented in detail by Whittam (34). It is quite possible that the selective pressure for the acquisition of such an array of genes enhancing pathogenicity has come about from the development of antibiotic resistant strains.

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