Genome Plasticity in Clinical Escherichia coli: Comparative Insights into Pathogenicity Islands, Prophages, and CRISPR–Cas Systems

Background. Escherichia coli is a common inhabitant of the human gastrointestinal tract but can also act as an opportunistic pathogen responsible for a wide range of clinical infections. Its remarkable genomic plasticity, driven by horizontal gene transfer and mobile genetic elements, enables rapid adaptation to different host environments. Understanding the structural genomic components that contribute to bacterial diversification is therefore essential for interpreting strain variability in clinical isolates. Methods. Clinical Escherichia coli isolates were recovered from different clinical specimens using standard microbiological identification methods. Based on preliminary characterization, six representative isolates were selected for whole-genome sequencing (WGS). Genomic analysis was performed to investigate structural genome features, including genome assembly characteristics, prophage regions, pathogenicity islands (PAIs), and CRISPR–Cas systems. Results. Out of 1000 clinical samples analyzed, 125 isolates (12.5%) were identified as Escherichia coli, with the highest isolation rate observed in urine samples (22.75%), reflecting its strong association with urinary tract infections. Genome assembly analysis revealed genome sizes ranging from 6.87 to 9.24 Mb with relatively conserved GC content (~50%). Comparative genomic analysis identified substantial variation in accessory genomic elements among isolates. Prophage regions ranged from 6 to 14 per genome and showed differences in structural completeness. Pathogenicity island analysis demonstrated that adhesion/fimbriae and siderophore-associated islands were the most abundant functional categories, whereas T3SS-associated islands were detected only in isolate E63. In contrast, CRISPR–Cas analysis showed a conserved Type I-E system across all isolates, with variation in spacer numbers and array counts. Conclusion. The analyzed E. coli isolates exhibit considerable structural genomic variability, mainly driven by differences in prophage content and pathogenicity islands. These mobile genetic elements play a key role in shaping genome plasticity and strain-level diversification, while CRISPR–Cas systems remain relatively conserved. The findings highlight the importance of accessory genome components in the evolutionary adaptation of clinical   E. coli populations. These findings provide genomic insights into the evolution of clinically relevant E.coli lineages and support the integration of WGS in surveillance programs.