Escherichia albertii Pathogenesis.

Escherichia albertii is an emerging enteropathogen of humans and many avian species. This bacterium is a close relative of Escherichia coli and has been frequently misidentified as enteropathogenic or enterohemorrhagic E. coli due to their similarity in phenotypic and genetic features, such as various biochemical properties and the possession of a type III secretion system encoded by the locus of enterocyte effacement. This pathogen causes outbreaks of gastroenteritis, and some strains produce Shiga toxin. Although many genetic and phenotypic studies have been published and the genome sequences of more than 200 E. albertii strains are now available, the clinical significance of this species is not yet fully understood. The apparent zoonotic nature of the disease requires a deeper understanding of the transmission routes and mechanisms of E. albertii to develop effective measures to control its transmission and infection. Here, we review the current knowledge of the phylogenic relationship of E. albertii with other Escherichia species and the biochemical and genetic properties of E. albertii, with particular emphasis on the repertoire of virulence factors and the mechanisms of pathogenicity, and we hope this provides a basis for future studies of this important emerging enteropathogen.

Genomic Properties and Temporal Analysis of the Interaction of an Invasive Escherichia albertii With Epithelial Cells.

Diarrhea is one of the main causes of infant mortality worldwide, mainly in the developing world. Among the various etiologic agents, Escherichia albertii is emerging as an important human enteropathogen. E. albertii promote attaching and effacing (AE) lesions due to the presence of the locus of enterocyte effacement (LEE) that encodes a type three secretion system (T3SS), the afimbrial adhesin intimin and its translocated receptor, Tir, and several effector proteins. We previously showed that E. albertii strain 1551-2 invades several epithelial cell lineages by a process that is dependent on the intimin-Tir interaction. To understand the contribution of T3SS-dependent effectors present in E. albertii 1551-2 during the invasion process, we performed a genetic analysis of the LEE and non-LEE genes and evaluated the expression of the LEE operons in various stages of bacterial interaction with differentiated intestinal Caco-2 cells. The kinetics of the ability of the 1551-2 strain to colonize and form AE lesions was also investigated in epithelial HeLa cells. We showed that the LEE expression was constant during the early stages of infection but increased at least 4-fold during bacterial persistence in the intracellular compartment. An in silico analysis indicated the presence of a new tccP/espFU subtype, named tccP3. We found that the encoded protein colocalizes with Tir and polymerized F-actin during the infection process in vitro. Moreover, assays performed with Nck null cells demonstrated that the 1551-2 strain can trigger F-actin polymerization in an Nck-independent pathway, despite the fact that TccP3 is not required for this phenotype. Our study highlights the importance of the T3SS during the invasion process and for the maintenance of E. albertii 1551-2 inside the cells. In addition, this work may help to elucidate the versatility of the T3SS for AE pathogens, which are usually considered extracellular and rarely reach the intracellular environment.

Genomic properties and temporal analysis of the interaction of an invasive Escherichia albertii with epithelial cells

Diarrhea is one of the main causes of infant mortality worldwide, mainly in the developing world. Among the various etiologic agents, Escherichia albertii is emerging as an important human enteropathogen. E. albertii promote attaching and effacing (AE) lesions due to the presence of the locus of enterocyte effacement (LEE) that encodes a type three secretion system (T3SS), the afimbrial adhesin intimin and its translocated receptor, Tir, and several effector proteins. We previously showed that E. albertii strain 1551-2 invades several epithelial cell lineages by a process that is dependent on the intimin-Tir interaction. To understand the contribution of T3SS-dependent effectors present in E. albertii 1551-2 during the invasion process, we performed a genetic analysis of the LEE and non-LEE genes and evaluated the expression of the LEE operons in various stages of bacterial interaction with differentiated intestinal Caco-2 cells. The kinetics of the ability of the 1551-2 strain to colonize and form AE lesions was also investigated in epithelial HeLa cells. We showed that the LEE expression was constant during the early stages of infection but increased at least 4-fold during bacterial persistence in the intracellular compartment. An in silico analysis indicated the presence of a new tccP/espFU subtype, named tccP3. We found that the encoded protein colocalizes with Tir and polymerized F-actin during the infection process in vitro. Moreover, assays performed with Nck null cells demonstrated that the 1551-2 strain can trigger F-actin polymerization in an Nck-independent pathway, despite the fact that TccP3 is not required for this phenotype. Our study highlights the importance of the T3SS during the invasion process and for the maintenance of E. albertii 1551-2 inside the cells. In addition, this work may help to elucidate the versatility of the T3SS for AE pathogens, which are usually considered extracellular and rarely reach the intracellular environment.

Phenotypic characterization and virulence-related properties of Escherichia albertii strains isolated from children with diarrhea in Brazil.

Escherichia albertii are emerging enteropathogens, whose identification is difficult, as they share biochemical characteristics and some virulence-related genes with diarrheagenic Escherichia coli (DEC). Studies on phylogeny, phenotypic characteristics and potential virulence factors of human E. albertii strains are scarce. In this study, we identified by multiplex PCR five E. albertii among 106 strains isolated from diarrheic children in São Paulo, Brazil, which were previously classified as atypical enteropathogenic E. coli. All strains were investigated regarding their phylogeny, biochemical properties, virulence-related properties, antimicrobial resistance and presence of putative virulence-related genes. All strains belonged to different E. albertii lineages and adhered to and produced attaching and effacing lesions on HeLa cells. Three strains invaded Caco-2 cells, but did not persist intracellularly, and three formed biofilms on polystyrene surfaces. All strains were resistant to few antibiotics and only one carried a self-transmissible resistance plasmid. Finally, among 38 DEC and 18 extraintestinal pathogenic E. coli (ExPEC) virulence-related genes searched, six and three were detected, respectively, with paa and cdtB being found in all strains. Despite the limited number of strains, this study provided additional knowledge on human E. albertii virulence potential, showing that they share important virulence factors with DEC and ExPEC.

Complete Genome Sequence of Escherichia albertii Strain 1551-2, a Potential Extracellular and Intracellular Pathogen.

Escherichia albertii has recently been recognized as an emerging human and bird enteric pathogen. Here, we report the complete chromosome sequence of a clinical isolate of E. albertii strain 1551-2, which may provide information about the pathogenic potential of this new species and the mechanisms of evolution of Escherichia species.