A virulent parent with probiotic progeny: comparative genomics of Escherichia coli strains CFT073, Nissle 1917 and ABU 83972

• DOI: 10.1007/s00438-010-0532-9
• Publication Date: 2010-03-30T07:05:11Z
• Authors: Rebecca Munk Vejborg; Carsten Friis; Viktoria Hancock; Mark A. Schembri; Per Klemm
• Keywords: Identification; 570; Pathogenicity islands; Genomic Islands; Virulence Factors; Prophages; CFT073; Persistence; 03 medical and health sciences; 1311 Genetics; Capsular polysaccharide synthesis; 1312 Molecular Biology; Escherichia coli; Cluster Analysis; Gene-expression; Biofilm formation; Selection; ABU 83972; Urinary tract infection; Comparative Genomic Hybridization; 0303 health sciences; Urinary-tract-infection; Probiotics; Epithelial-cells; Bacterial; Comparative genomic hybridization analysis; Genetic Variation; Reproducibility of Results; Gene Expression Regulation, Bacterial; Genomics; Nissle 1917; 3. Good health; Phenotype; Gene Expression Regulation; Genes; Genes, Bacterial; Asymptomatic bacteriuria

Escherichia coli is a highly versatile species encompassing a diverse spectrum of strains, i.e. from highly virulent isolates causing serious infectious diseases to commensals and probiotic strains. Although much is known about bacterial pathogenicity in E. coli, the understanding of which genetic determinants differentiates a virulent from an avirulent strain still remains limited. In this study we designed a new comparative genomic hybridization microarray based on 31 sequenced E. coli strains and used it to compare two E. coli strains used as prophylactic agents (i.e. Nissle 1917 and 83972) with the highly virulent uropathogen CFT073. Only relatively minor genetic variations were found between the isolates, suggesting that the three strains may have originated from the same virulent ancestral parent. Interestingly, Nissle 1917 (a gut commensal strain) was more similar to CFT073 with respect to genotype and phenotype than 83972 (an asymptomatic bacteriuria strain). The study indicates that genetic variations (e.g. mutations) and expression differences, rather than genomic content per se, contribute to the divergence in disease-causing ability between these strains. This has implications for the use of virulence factors in epidemiological research, and emphasizes the need for more comparative genomic studies of closely related strains to compare their virulence potential.