The Evolutionary History of Shigella and Enteroinvasive Escherichia coli Revised

Abstract

In Shigella and enteroinvasive Escherichia coli (EIEC), the etiologic agents of shigellosis in humans, the determinants responsible for entry of bacteria into and dissemination within epithelial cells are encoded by a virulence plasmid. To understand the evolution of the association between the virulence plasmid and the chromosome, we performed a phylogenetic analysis using the sequences of four chromosomal genes (trpA, trpB, pabB, and putP) and three virulence plasmid genes (ipaB, ipaD, and icsA) of a collection of 51 Shigella and EIEC strains. The phylogenetic tree derived from chromosomal genes showed a typical "star" phylogeny, indicating a fast diversification of Shigella and EIEC groups. Phylogenetic groups obtained from the chromosomal and plasmidic genes were similar, suggesting that the virulence plasmid and the chromosome share similar evolutionary histories. The few incongruences between the trees could be attributed to exchanges of fragments of different plasmids and not to the transfer of an entire plasmid. This indicates that the virulence plasmid was not transferred between the different Shigella and EIEC groups. These data support a model of evolution in which the acquisition of the virulence plasmid in an ancestral E. coli strain preceded the diversification by radiation of all Shigella and EIEC groups, which led to highly diversified but highly specialized pathogenic groups.

Gene and genome trees conflict at many levels

“…These were the Yersinia group, the Salmonella group and the Escherichia/ Shigella group. We did not find that there was a single origin of Shigella (Escobar-Paramo et al 2003), rather, we found multiple origins, in accordance with the findings of Pupo et al (2000). We did not find that the three groups were a single homogenous entity; we did find partitions.…”

Molecular Evolution of Pathogenicity-Island Genes in Pseudomonas viridiflava

“…While there is sound evidence that the evolution of pathogenesis involves the acquisition of virulence-related genes (including entire PAIs) via HGT (Reid et al 2000;Bukhalid et al 2002), some studies reported that PAIs have been retained within pathogen species over evolutionary time (e.g., Escobar-Paramo et al 2003;Gressmann et al 2005;Rohmer et al 2004;Nallapareddy et al 2005). We do not know why some PAIs are evolutionary stable whereas others are not, but our results provide one possible explanation: Unlike a PAI acquired via recent HGT, an evolutionary stable PAI can work as a large reservoir of preexisting genetic variation in this highly polymorphic species.…”

The Pangenome Structure ofEscherichia coli: Comparative Genomic Analysis ofE. coliCommensal and Pathogenic Isolates

“…Members of this pathovar bind to the epithelial layer in the small intestine and secrete toxins that cause an altered water balance in the intestinal lumen, resulting in watery diarrhea (49). While none of the other E. coli pathovars routinely invades the epithelial cells, members of the EIEC group readily enter the enterocytes of the colon and move laterally, thus avoiding many of the host innate immune responses (12,44). Clinically and diagnostically, EIEC is similar to Shigella species, sharing many of the same virulence factors (12,44).…”

“…While none of the other E. coli pathovars routinely invades the epithelial cells, members of the EIEC group readily enter the enterocytes of the colon and move laterally, thus avoiding many of the host innate immune responses (12,44). Clinically and diagnostically, EIEC is similar to Shigella species, sharing many of the same virulence factors (12,44). Overall, E. coli isolates and the diseases that they cause are diverse, and while many virulence factors are known for each of the different pathovars, the genetic content of these pathogens has not been examined previously on a genomic level.…”