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Objectives of this study are to determine the differences in clonality, virulence gene (VG) content and phylogenetic group between non extended-spectrum beta-lactamase-producing E. coli (non-ESBL-EC) and ESBL-EC isolates from urine.Patients and Methods: This study characterized a total of 100 clinical E. coli isolates consecutively obtained from the inpatients hospitalized in The First Affiliated Hospital of Ningbo University in China by polymerase-chain reaction (PCR).Results: Phylogenetic group B2 was found to be the most prevalent in both ESBL-EC and non-ESBL-EC group. Among 100 clinical isolates, the count of acquired virulence genes in group B2 was found to be significantly higher than that in group A, B1, and D (p < 0.001). Additionally, the presence of content within virulence genes (the total number of virulence genes detected per isolate) in B2 of non-ESBL-EC and ESBL-EC showed a significant difference (p< 0.001). ST131 was detected exclusively in ESBL-EC, while ST95 and ST73 were the main sequence types in non-ESBL-EC.Conclusion: Our study demonstrated the different distribution of MLST, phylogenetic group in ESBL-EC and non-ESBL-EC group. The inverse association between beta-lactamase resistance and VG content performed in this study should get a lot more attention. At the same time, we should also be wary of the appearance of non-ESBL-EC isolates of group B2 harboring more virulence genes which will lead to high pathogenicity. [ABSTRACT FROM AUTHOR]

Background: Sequence type 1193 is a new such lineage among fluoroquinolone-resistant Escherichia coli, which has risen dramatically within the last several years. However, reasons for rapid emergence and successful spread of E. coli ST1193 remain unclear. The aim of this study was to compare the pathogenicity and survivability features of E. coli ST1193 with global epidemic lineage, ST131. Methods: A total of 30 E. coli were used in this study. Isolates were divided into two groups, ST1193 (n=15) and ST131 (n=15). Adhesion and invasion to T24 cells and resistance to serum were quantified and compared among two groups. Biofilm formation capacity was assessed by crystal violet assay. Macrocolony formation was assessed on macrocolony formation plates. Resistance to hydrogen peroxide was performed by broth microdilution. RAW264.7 cells were used to assess the anti-phagocytic function of different isolates. Results: Adhesion and invasion assays revealed that E. coli ST1193 could adhere and invade T24 cells (p < 0.05). 93.3% of E. coli ST1193 could form biofilms. The majority of E. coli ST1193 (66.7%) possessed no curli/no cellulose on macrocolony formation plates. E. coli ST1193 showed significant growth in serum and hydrogen peroxide and illustrated higher anti-phagocytic function to RAW264.7 cells (p < 0.05). Group analysis showed that E. coli ST1193 was similar to ST131 in pathogenicity- and survivability-associated phenotypic characteristics (p > 0.05). Conclusion: Our study provided more insights into pathogenicity and survivability features of E. coli ST1193, which was similar to ST131. Our study could be of great importance in understanding the emergence of global spread E. coli ST1193. Strategic and continued surveillance should be carried out to prevent the infections caused by E. coli ST1193. [ABSTRACT FROM AUTHOR]