| Title | Whole-genome sequencing analysis of Shiga toxin-producing Escherichia coli O22:H8 isolated from cattle prediction pathogenesis and colonization factors and position in STEC universe phylogeny |
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| Author | Wanderson Marques Da Silva1*, Mariano Larzabal1, Flavia Figueira Aburjaile2, Nahuel Riviere1, Luisina Martorelli3, James Bono4, Ariel Amadio5, and Angel Cataldi1 |
| Address | 1Agrobiotechnology and Molecular Biology Institute (IABIMO-INTA/CONICET), Hurlingham B1686IGC, Argentina, 2Institute of Biological Sciences, Federal University of Minas Gerais (UFMG), Belo Horizonte 31270-901, Brazil, 3Institute of Veterinary Pathobiology (IPEVET-INTA/CONICET), Hurlingham B1686WAA, Argentina, 4U.S Meat Animal Research Center, Agricultural Research Service, U.S. Department of Agriculture, Clay Center, Nebraska 68933, USA, 5Dairy Chain Research Institute (IDICAL-INTA/CONICET), Rafaela 2300, Santa Fe S2300, Argentina |
| Bibliography | Journal of Microbiology, 60(7),689-704, 2022, |
| DOI | 10.1007/s12275-022-1616-z |
| Key Words | non-LEE STEC, non-O157, bacterial genome, pangenome, foodborne pathogen, genomic island, T6SS |
| Abstract | Shiga toxin-producing Escherichia coli (STEC) is a foodborne pathogen capable of causing illness in humans. In a previous study, our group showed that a STEC isolate belonging to O22:H8 serotype (strain 154) can interfere with STEC O157:H7 colonization both in vitro and in vivo. Using whole-genome sequencing and genomic comparative, we predicted a subset of genes acquired by O22:H8 strain 154 through horizontal gene transfer that might be responsible for the phenotype previously described by our group. Among them were identified genes related to the pathogenesis of non-LEE (locus of enterocyte effacement) STEC, specific metabolic processes, antibiotic resistance and genes encoding for the T6SS-1 that is related to inter-bacterial competition. In addition, we showed that this strain carries stx1c and stx2dact, a mucus-inducible variant. The results obtained in this study provide insights into STEC genomic plasticity and the importance of genomic islands in the adaptation and pathogenesis of this pathogen. |