Endometrial pathogenic Escherichia coli in canine pyometra: severity of tissue damage, host defense evasion, and antimicrobial resistance profile

<i>Escherichia coli</i> (<i>E. coli</i>) is the bacterium most frequently isolated from canine pyometra. The Endometrial Pathogenic <i>E. coli</i> (EnPEC) show virulence traits that cause tissue damage through adhesion/invasion of cells, and toxin production. Phosphoinositide 3-kinases (PI3K) are intracellular signal transducers with a fundamental role in the innate immune defense. Bacteria that inhibit the PI3K pathway can escape the host defenses. The aim of this study was (a) to investigate the association among the characteristics of <i>E. coli</i> isolated from pyometra (phylogroup, hemolysis, CNF-cytotoxic necrotizing factor, CDT-cytolethal distending toxin), the severity of tissue lesions and the expression of PI3K; (b) to assess the resistance profile. <i>E. coli</i> was isolated from 17/21 uteri, always in pure culture. All <i>E. coli</i> belonged to the phylogroup B2 and 12/17 uteri contained hemolytic strains. CNF was evidenced only in the hemolytic strains. CDT was never detected. Four uteri showed perforation: all contained CNF-positive hemolytic <i>E. coli</i> and PI3K expression was negative. No significant association was found between the characteristics of <i>E. coli</i> and the degree of tissue damage or PI3K expression. The non-hemolytic <i>E. coli</i> tended to show higher resistance toward some antimicrobials. Our results confirm that the highly virulent phylogenetic group B2 is often involved in canine pyometra. PI3K was not expressed in the perforated uteri, suggesting a potential interference of the pathogen with the host cells defenses. Future research should be focused on the mechanism of host defense evasion through the inactivation of the PI3K signaling pathway.