Phylogenetic relationships, biofilm formation, motility, antibiotic resistance and extended virulence genotypes among Escherichia coli strains from women with community-onset primitive acute pyelonephritis

Abstract

The present work set out to search for a virulence repertoire distinctive for Escherichia coli causing primitive acute pyelonephritis (APN). To this end, the virulence potential of 18 E. coli APN strains was genotypically and phenotypically assessed, comparatively with 19 strains causing recurrent cystitis (RC), and 16 clinically not significant (control, CO) strains. Most of the strains belong to phylogenetic group B1 (69.8%; p<0.01), and APN strains showed unique features, which are the presence of phylogroup A, and the absence of phylogroup B2 and non-typeable strains. Overall, the most dominant virulence factor genes (VFGs) were ecpA and fyuA (92.4 and 86.7%, respectively; p<0.05), and the mean number of VFGs was significantly higher in uropathogenic strains. Particularly, papAH and malX were exclusive for uropathogenic strains. APN and RC strains showed a significantly higher prevalence of fyuA, usp, and malX than of CO strains. Compared to RC strains, APN ones showed a higher prevalence of iha, but a lower prevalence of iroN, cnf1, and kpsMT-II. Hierarchical cluster analysis showed a higher proportion of two gene clusters (malX and usp, and fyuA and ecpA) were detected in the APN and RC groups than in CO, whereas iutA and iha clusters were detected more frequently in APN strains. The motility level did not differ among the study-groups and phylogroups considered, although a higher proportion of swarming strains was observed in APN strains. Antibiotic-resistance rates were generally low except for ampicillin (37.7%), and were not associated with specific study- or phylogenetic groups. APN and RC strains produced more biofilm than CO strains. In APN strains, iha was associated with higher biofilm biomass formation, whereas iroN and KpSMT-K1 were associated with a lower amount of biofilm biomass. Further work is needed to grasp the virulence and fitness mechanisms adopted by E. coli causing APN, and hence develop new therapeutic and prophylactic approaches.

Virulence factors of uropathogenic Escherichia coli (UPEC) and correlation with antimicrobial resistance

“…Several studies done in the past also conclude the same findings [30, 31]. Pompilio et al [32] concluded that, although antimicrobial resistance was higher in biofilm producers, the difference was statistically non-significant. Protection of microorganism from host immunity, insufficient antimicrobial concentration and delayed penetration into the deeper layers of biofilms are the major reasons for antibiotic resistance in biofilm structures [22].…”

Characterization of native Escherichia coli populations from bovine vagina of healthy heifers and cows with postpartum uterine disease

“…Genome plasticity is the main driver of E. coli phenotypic diversity and evolution [48]; thus, this dynamism is responsible for the relevant differences observed among the pathogenic strains associated with diseases [49]. In the present study, the genomic diversity among vaginal E. coli was assessed through the ERIC-PCR technique as previously applied for animal samples taken from different mucosae [50,51].…”

Relationship between Virulence and Resistance among Gram-Negative Bacteria

“…The clearest example of this is found in uropathogenic strains of E. coli (UPEC). These strains possess certain virulence factors that allow them to colonize the urinary tract and produce cystitis (CT), pyelonephritis (PNP) and prostatitis (PT), and they can even reach the blood stream [ 17 ]. Many of these virulence factors, such as hemolysin, cytotoxic necrotizing factor, P-fimbriae, siderophore systems, S-fimbriae, yersiniabactin, toxin autotransporters, among others, are in regions of the chromosome called pathogenicity islands (PAIs) [ 18 ].…”