Shiga toxin-producing Escherichia coli (STEC) strains are significant public health threats due to their association with severe gastrointestinal diseases, including hemorrhagic colitis and hemolytic uremic syndrome (HUS). E. coli O26 is one of the non-O157 STEC strains that has emerged as a prominent pathogen. Comparative genomics of E. coli O26 with other STEC strains, particularly E. coli O157:H7, provides insights into the genetic diversity, evolution, and pathogenic mechanisms of these bacteria.
Core and Accessory Genomes
The genomic structure of STEC strains consists of a core genome, which includes genes shared by all strains, and an accessory genome, which comprises strain-specific genes acquired through horizontal gene transfer (HGT). The core genome encodes essential functions for bacterial survival and reproduction, while the accessory genome often contains genes related to virulence, antibiotic resistance, and adaptation to specific niches.
E. coli O26 and other STEC strains share a considerable portion of their core genomes, reflecting their common evolutionary origins. However, the accessory genomes of these strains exhibit significant variability, contributing to differences in virulence and epidemiology. Comparative genomic studies have identified various pathogenicity islands (PAIs), plasmids, and prophages in the accessory genomes of STEC strains, which play crucial roles in their pathogenicity.
Shiga Toxins and Virulence Factors
Shiga toxins (Stx) are the primary virulence factors of STEC strains. These toxins are encoded by stx genes located on lambdoid prophages. The two main types of Shiga toxins, Stx1 and Stx2, are potent inhibitors of protein synthesis in host cells, leading to cellular damage and inflammation. Comparative genomics reveals differences in the presence and types of stx genes among STEC strains.
E. coli O157:H7 typically carries stx2 genes, which are associated with more severe disease outcomes. In contrast, E. coli O26 may harbor either stx1 or stx2 genes, or both, contributing to its pathogenic potential. The variability in stx gene content among STEC strains underscores the importance of genetic diversity in their virulence.
Pathogenicity Islands (PAIs)
Pathogenicity islands are large genomic regions acquired through HGT that encode clusters of virulence genes. One of the well-known PAIs in STEC strains is the locus of enterocyte effacement (LEE), which is crucial for the formation of attaching and effacing (A/E) lesions on host intestinal cells. The LEE encodes the type III secretion system (T3SS), intimin, and various effector proteins.
Comparative genomics of E. coli O26 and E. coli O157:H7 reveals similarities and differences in their PAIs. Both strains possess the LEE, but the sequence and gene content of the LEE can vary. Additionally, E. coli O26 may contain unique PAIs not present in E. coli O157:H7, contributing to strain-specific differences in virulence and host interactions.
Plasmids and Antibiotic Resistance
Plasmids are extrachromosomal DNA elements that often carry genes related to virulence, antibiotic resistance, and metabolic functions. STEC strains, including E. coli O26 and E. coli O157:H7, frequently harbor plasmids that enhance their pathogenic potential. Comparative genomics has identified plasmid-encoded virulence factors, such as hemolysins, adhesins, and additional T3SS effectors.
Antibiotic resistance is a growing concern for STEC infections. Plasmids play a significant role in the dissemination of antibiotic resistance genes among bacterial populations. Comparative genomic studies reveal that E. coli O26 and other STEC strains may carry plasmids with genes conferring resistance to multiple antibiotics, complicating treatment options.
Evolution and Genetic Diversity
The evolution of STEC strains is driven by a combination of clonal expansion, mutation, and HGT. Comparative genomics provides insights into the genetic diversity and evolutionary history of these pathogens. E. coli O26 and other STEC strains exhibit high levels of genetic diversity, reflecting their adaptation to different environments and hosts.
Phylogenetic analysis based on whole-genome sequencing reveals that STEC strains form distinct clades, with E. coli O26 belonging to a separate lineage from E. coli O157:H7. This genetic diversity underscores the importance of surveillance and monitoring efforts to track the emergence and spread of different STEC strains.
Conclusion
Comparative genomics of E. coli O26 and other Shiga toxin-producing strains offers valuable insights into their genetic diversity, evolution, and pathogenic mechanisms. While these strains share a core genome, their accessory genomes exhibit significant variability, contributing to differences in virulence and epidemiology. Understanding the genetic basis of STEC pathogenicity is essential for developing effective strategies to prevent and control infections. Continued research in this field will enhance our ability to combat these formidable pathogens and mitigate their impact on public health.
