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Category: Bacterial Pathogenesis
Thomas Whittam, Shiga Toxin-Producing Escherichia coli, and the Clinical Consequences of Clonality, Page 1 of 2
< Previous page | Next page > /docserver/preview/fulltext/10.1128/9781555817114/9781555819354_Chap15-1.gif /docserver/preview/fulltext/10.1128/9781555817114/9781555819354_Chap15-2.gifAbstract:
This chapter reviews the impact of Tom's contributions to the field of microbial evolution and to the evolution of one's understanding of the enteric pathogenicity of E. coli. Additional progress was made, also in Germany, in the 1920s: Adam demonstrated groups of E. coli that were biochemically distinct, which he termed ‘’dyspepsiekoli’’. The resulting genetic analysis categorized the species into four main groups (A, B1, B2, and D) and one minor group (E), and generated a widely used phylogenetic reference that has served as the foundation for investigators in the generation since. The putative cardinal virulence trait of E. coli O157:H7, namely, the possession of one or more Shiga toxin genes, was not by itself sufficient to cause severe human disease. The author says that Tom also identified different eae (intimin) alleles as different classes of EPEC and Shiga toxin-producing E. coli (STEC) were described, and framed his work in the context of microbial evolution, epidemiology, and clinical medicine. Despite these limitations, Tom expounded graciously and patiently on his theories of clonality. Tom's investigations into the emergence of diarrheagenic E. coli, and most particularly of the O157:H7 EHEC 1 clade, stand as monumental and enduring contributions to the field.
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Early presentation on EHEC by Tom Whittam. (Left) Abstract book cover. (Right) Abstract of talk delivered by Tom Whittam on the afternoon of Tuesday, July 14, 1987.
Unexplained faint band in a gel. Primers within yehV in E. coli O55:H7 produced a prominent 340-bp amplicon (white oval) as expected because this gene is not disrupted by a bacteriophage. Primers across the same site in stx 1 – stx 2 + as well as stx 1 – stx 2 + E. coli O157:H7 yield fainter bands (black oval), whereas we anticipated a stronger band, as in the nontoxigenic progenitor strain, E. coli O55:H7, amplified using the same primer set. Subsequent work demonstrated that a truncated bacteriophage occupied this site in E. coli O157:H7 that did not contain stx 1 (black dashed oval); the bacteriophage-chromosome junction amplicons are within the white dashed borders. Additional amplifications led us to deduce the precise phylogeny of emergence of the three major E. coli O157: H7 subgroups ( 14 , 56 , 87 , 88 ). These data eventually led us to formulate a precise emergence of the EHEC 1 clade (see Fig. 3 ). Reproduced with permission from Fig. 1 in reference 88 .
Evolutionary scenario for EHEC 1 pathogens. E. coli O55:H7 belongs to the most ancestral subgroup (A) of the EHEC 1 clade. The second sphere from the left (lower row) depicts a probably extinct intermediate between O55:H7 and E. coli expressing the O157 lipopolysaccharide (LPS), with subgroup B consisting of the sorbitol-fermenting O157:H– and subgroup C consisting of E. coli O157:H7. We note several critical intraclade events. The ovals within clusters represent genomically sequenced strains (middle gray). Strains used for single nucleotide polymorphism (SNP) consensus sampling are black, inferred founders are light gray, and postulated organisms that are immediate progenitors to the next cluster or subgroup are white ovals. In cluster 1, screened strains were assigned to the main branch if they had each of the three signature SNPs among the 111 shared SNPs ( 38 / 48 ), and the minor branch if they lacked this set of SNPs ( 10 / 48 ). More extensive evolutionary detail is provided in Fig. S1 in reference 56 . Distances not drawn to scale. Reprinted with permission from reference 56 . GUD, β-d-glucuronidase; TAI, tellurite resistance- and adherence-conferring island.