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Recently, Escherichia albertii has been identified as a causative agent of diarrhea in humans and is often misidentified as diarrheagenic Escherichia coli (DEC), a lactose-nondegrading bacterium. In this study, we performed biochemical characterization, gene possession status, drug susceptibility testing, and sequencing analysis of the strains detected in urine samples. One urea-degrading strain was detected in terms of biochemical characteristics, but was found to be nonurea-degrading by another method, leading to conflicting results. All target strains possessed the E. albertii-specific gene, the DEC common gene eae, and the E. coli 16S rRNA gene. In the drug susceptibility test, all urine-derived strains were sensitive to tetracycline (TC), whereas the JCM 17328 strain was resistant to TC, suggesting that TC is effective against urine-derived E. albertii strains. In 16S rRNA sequencing analysis, the E. albertii strains were ranked at the top of homology, but not in the top one, making it difficult to differentiate them from other strains. In summary, if a suspected lactose-nondegrading E. coli strain was isolated from a urine sample, it could be differentiated from E. albertii by the presence of E. albertii-specific genes. [ABSTRACT FROM AUTHOR]

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The toxigenic conversion of Escherichia coli strains by Shiga toxin-converting (Stx) bacteriophages were prominent and recurring events in the stepwise evolution of enterohemorrhagic E. coli (EHEC) O157:H7 from an enteropathogenic (EPEC) O55:H7 ancestor. Atypical, attenuated isolates have been described for both non-sorbitol fermenting (NSF) O157:H7 and SF O157:NM serotypes, which are distinguished by the absence of Stx, the characteristic virulence hallmark of Stx-producing E. coli (STEC). Such atypical isolates either never acquired Stx-phages or may have secondarily lost stx during the course of infection, isolation, or routine subculture; the latter are commonly referred to as LST (Lost Shiga Toxin)-isolates. In this study we analyzed the genomes of 15 NSF O157:H7 and SF O157:NM strains from North America, Europe, and Asia that are characterized by the absence of stx , the virulence hallmark of STEC. The individual genomic basis of the Stx (−) phenotype has remained largely undetermined as the majority of STEC genomes in public genome repositories were generated using short read technology and are in draft stage, posing a major obstacle for the high-resolution whole genome sequence typing (WGST). The application of LRT (long-read technology) sequencing provided us with closed genomes, which proved critical to put the atypical non-shigatoxigenic NSF O157:H7 and SF O157:NM strains into the phylogenomic context of the stepwise evolutionary model. Availability of closed chromosomes for representative Stx (−) NSF O157:H7 and SF O157:NM strains allowed to describe the genomic basis and individual evolutionary trajectories underlying the absence of Stx at high accuracy and resolution. The ability of LRT to recover and accurately assemble plasmids revealed a strong correlation between the strains' featured plasmid genotype and chromosomally inferred clade, which suggests the coevolution of the chromosome and accessory plasmids. The identified ancestral traits in the pSFO157 plasmid of NSF O157:H7 strain LSU-61 provided additional evidence for its intermediate status. Taken together, these observations highlight the utility of LRTs for advancing our understanding of EHEC O157:H7/NM pathogenome evolution. Insights into the genomic and phenotypic plasticity of STEC on a lineage- and genome-wide scale are foundational to improve and inform risk assessment, biosurveillance, and prevention strategies. [ABSTRACT FROM AUTHOR]

In 1987, cytolethal distending toxin (CDT) was discovered by Johnson and Lior as a new type of protein toxin produced by certain strains of Escherichia coli, which is different from heat-labile enterotoxin (LT) produced by enterotoxigenic E. coli. Although LT causes only cell elongation, CDT causes cell elongation, cell distention, irreversible cell cycle arrest, and consequently, death of the cultured mammalian cells. Recently, CDT was recognized as a new family of bacterial toxin, as a genotoxin, produced by a diverse group of gram-negative bacteria, all of which are related to mucosal infection. Although tremendous efforts have been made to study the structure and mode of action of CDT, its role in bacterial pathogenesis still remains unclear. In this review, we focus mainly on CDT produced by enteric bacteria and describe the history of CDT, their gene and protein structure, structure-function relationship, and its mode of action particularly how CDT contributes to the gastrointestinal infections. [ABSTRACT FROM AUTHOR]