| Summary: | <p>Abstract</p> <p>Background</p> <p>Previous studies have established a correlation between electrophoretic polymorphism of esterase B, and virulence and phylogeny of <it>Escherichia coli</it>. Strains belonging to the phylogenetic group B2 are more frequently implicated in extraintestinal infections and include esterase B<sub>2 </sub>variants, whereas phylogenetic groups A, B1 and D contain less virulent strains and include esterase B<sub>1 </sub>variants. We investigated esterase B as a marker of phylogeny and/or virulence, in a thorough analysis of the esterase B-encoding gene.</p> <p>Results</p> <p>We identified the gene encoding esterase B as the acetyl-esterase gene (<it>aes</it>) using gene disruption. The analysis of <it>aes </it>nucleotide sequences in a panel of 78 reference strains, including the <it>E. coli </it>reference (ECOR) strains, demonstrated that the gene is under purifying selection. The phylogenetic tree reconstructed from <it>aes </it>sequences showed a strong correlation with the species phylogenetic history, based on multi-locus sequence typing using six housekeeping genes. The unambiguous distinction between variants B<sub>1 </sub>and B<sub>2 </sub>by electrophoresis was consistent with Aes amino-acid sequence analysis and protein modelling, which showed that substituted amino acids in the two esterase B variants occurred mostly at different sites on the protein surface. Studies in an experimental mouse model of septicaemia using mutant strains did not reveal a direct link between <it>aes </it>and extraintestinal virulence. Moreover, we did not find any genes in the chromosomal region of <it>aes </it>to be associated with virulence.</p> <p>Conclusion</p> <p>Our findings suggest that <it>aes </it>does not play a direct role in the virulence of <it>E. coli </it>extraintestinal infection. However, this gene acts as a powerful marker of phylogeny, illustrating the extensive divergence of B2 phylogenetic group strains from the rest of the species.</p>
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