Molecular and Phenotypic Characterization of Escherichia coli Associated with Granulomatous Colitis of Boxer Dogs

Abstract

Invasive <i>Escherichia coli</i> is causally associated with granulomatous colitis (GC) of Boxer dogs and French Bulldogs. The virulence determinants of GC <i>E. coli</i> are unclear. <i>E. coli</i> isolated from 16 GC (36 strains) and 17 healthy control (HC: 33 strains) dogs were diverse in phylogeny, genotype, and serotype and lacked diarrheagenic genes. Genes encoding type II (<i>gsp</i>), IV (<i>traC</i>), and VI (<i>hcp</i>) secretion systems, long polar fimbriae (<i>lpfA</i>154/141), and iron acquisition (<i>fyuA</i>, <i>chuA</i>) were frequent in GC and HC. <i>E. coli</i> from 14/15 GC and 10/11 HC invaded Caco-2 better than non-pathogenic <i>E. coli</i> strain DH5α, with invasion correlated with motility and presence of <i>chuA</i> and <i>colV</i>. <i>E. coli</i> from all GC and 10/11 HC survived better than DH5α in J774 macrophages, with adherent-invasive <i>E. coli</i> (AIEC) in 60% GC and 73% HC. AIEC replicated in monocyte derived macrophages from a GC Boxer with CD48/SLAM risk haplotype but not the HC. Fluroquinolone resistant <i>E. coli</i> were less motile and invasive than fluoroquinolone sensitive (<i>p</i> < 0.05), and only 1/8 resistant strains met criteria for AIEC. In conclusion GC <i>E. coli</i> are diverse, resemble extraintestinal pathogenic <i>E. coli</i> (ExPEC), including AIEC, and can replicate in GC-susceptible macrophages. They are likely resident pathosymbionts that can opportunistically persist within macrophages of a GC-susceptible dog.