coli ( Sheikh et al., 2001 Sherlock et al., 2004 Schiebel et al., 2017) and in adherent-invasive E. coli, biofilm involvement in pathogenesis has been well defined in diarrheagenic E. Likewise, chronic Pseudomonas aeruginosa lung infections in cystic fibrosis patients are caused by biofilm-growing mucoid isolates ( Høiby et al., 2010).Ĭoncerning Escherichia coli, which can exist as a harmless commensal in the mammalian digestive tract and as a pathogen causing significant morbidity and mortality worldwide, its ability to form biofilm has been extensively studied from non-pathogenic E. Thus, it was shown that persistence of staphylococcal infections related to foreign bodies is due to biofilm formation ( Sabaté Brescó et al., 2017). Accordingly, biofilm-growing bacteria cause chronic infections, persisting inflammation, tissue damage, and foreign body infections ( Høiby et al., 2011). Bacterial biofilms are known for their resistance to antibiotics, disinfectants, and components of the innate and adaptative inflammatory defense system of the body ( Høiby et al., 2011). (1978) 30 years ago, it is well established that the majority of bacteria found in nature exists attached to surfaces within the structured biofilm ecosystem ( Costerton et al., 1978 Hall-Stoodley et al., 2004). Since the first definition of biofilms provided by Costerton et al. These isolates belong to a few clones previously described in various studies as dominant gut colonizers in mammalians and birds and comprised the B2-CH40-22-ST131 clone, i.e., the ancestor of the globally disseminated B2-CH40-30-ST131 clone that is the dominant clone among the weak biofilm producers. Clone, some VF, and FimB were associated with EBF, with clonal lineage being able to explain 72% of the variability of EBF.Ĭonclusion: Among our 394 isolates, <10% are able to quickly and persistently produce high biofilm levels over 5 h.
FimB-P2 variant was associated with G1 ( P = 0.0011) and FimB-P1 variant was associated with G3 ( P = 0.0023). VF mean was higher among G1 than among G3 isolates ( P < 0.001). B2-CH40-30-ST131 clone was associated with G3 ( P < 0.0001) and accounted for 25.5% of G3 isolates. The 394 isolates displayed 153 clones, of which 31 included at least three isolates. Phylogroup B2 displayed by 51.3% of the 394 isolates was more frequent in G1 (77.8%) than in G3 (47.6%) ( P = 0.0006). As CEC and ESBLEC isolates showed similar individual EBF kinetics in each group, a comparison of isolate features between each group was applied to gathered CEC and ESBLEC isolates after 2 h of incubation, 2 h being the most representative time point of the CEC and ESBLEC isolate segregation into the three groups. At 2 h, strong producers were more frequent among CEC ( n = 28 14.3%) than among ESBLEC ( n = 8 4%) ( P = 0.0004). Result: According to both biofilm production levels at 2, 3, and 5 h, and EBF kinetics over 5 h, CEC and ESBLEC isolates segregated into three EBF groups: strong (G1), moderate (G2), and weak (G3) producers. Then, biofilm-forming ability was contrasted with phylogroups, clonotypes ( fumC- fimH), and sequence types (STs), all being used to define clones, virulence factors (VF), and FimB.
Here, we assessed the early biofilm formation (EBF), i.e., adhesion stage, using the BioFilm Ring Test ® on 394 E.
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