Virulence characteristics of adherent-invasive Escherichia coli isolated from healthy individuals, patients and the environment (#8)
Collectively, ulcerative colitis (UC) and Crohn’s disease (CD) constitute idiopathic inflammatory bowel disease (IBD). While the pathogenic mechanisms underlying IBD remain poorly characterized, Escherichia coli has been implicated as a microbiological factor in disease pathogenesis. Increased numbers of mucosa-associated E. coli have consistently been identified in the gut of patients with IBD and colorectal cancer (CRC). Designated as adherent-invasive E. coli (AIEC), these strains show an enhanced ability to diffusely adhere (DA) to-, and invade intestinal epithelial cells (IECs), along with the ability to survive and replicate within macrophages. It has been shown that AIEC strains harbor specific virulence genes (VGs) associated with their pathogenicity. We investigated the presence of E. coli clones carrying phenotypic and genotypic traits consistent with AIEC among 808 diffusely adherent E. coli strains isolated from healthy individuals (HI), patients with community-acquired (CA) UTI, hospitalized patients with septicemia or urosepsis, sewage treatment plants (STPs) and surface waters (SW). Typing of the isolates, including phylogenetic grouping showed that they belonged to 48 common clones (CCs). Representatives of each of the CC were tested for their ability to invade Caco-2 cells, survive and replicate within macrophages, and the presence of six AIEC-associated VGs. Thirty-three percent of the isolates, belonging to 20 CCs, showed the ability to survive and replicate within macrophages, whilst containing the genes dsbA, htrA and clbA. These strains were sourced primarily from HI and CA-UTI patients (7 CCs each) and STPs (4 CCs). CA-UTI strains showed a significantly (P<0.001) higher intracellular bacterial load (6,929 ± 557 c.f.u. well-1) than others. Two CCs of the AIEC from CA-UTI patients and HI (one each) were found in five out of the six sources investigated. High presence of AIEC strains found in the gut of HI, not only implies their involvement in pathogenesis of CA-UTI, but also suggests the survival of these strains in STPs and the environment.