Serum resistance among Escherichia coli strains causing urinary tract infection in relation to O type and the carriage of hemolysin, colicin, and antibiotic resistance determinants

Abstract

The sensitivity to normal human serum of 91 smooth strains of Escherichia coli isolated from urinary tract infections was determined. Production of hemolysin, which was common and associated primarily with the types 04, 06, 018, and 075, was significantly correlated with high levels of serum resistance, both within the total population and within individual 0 types. In contrast, serum resistance was not significantly associated with antibiotic resistance (whether transmissible or not), with colicinogeny in general, or with colicin V production in particular. This indicates that the carriage of R and ColV plasmids, shown previously to be capable of conferring increased levels of serum resistance on individual strains of E. coli isolated from other sources, does not play an important part in determining the serum sensitivity of the E. coli population involved in urinary tract infection.

Distribution of the usp Gene in Uropathogenic Escherichia coli Isolated from Companion Animals and Correlation with Serotypes and Size‐Variations of the Pathogenicity Island

“…Seven virulence factors (VFs), including type 1 pilus (pil), pilus associated with pyelonephritis (pap), S fimbriae (sfa), afimbrial adhesin I (afaI), hemolysin (hly), aerobactin (aer) and cytotoxic necrotizing factor 1 (cnfI) have been documented to play an important role in causing human UTI (2). Several serotypes such as O1, O2, O4, O6, O8, O16, O18, O22, O25 and O75 are preferentially associated with UPEC strains and each of the uropathogenic virulence factors is significantly associated with these serotypes (1,6,8). E. coli strains isolated from dogs and cats with UTI have high prevalence of hly and clustered in 5 serotypes including O2, O4, O6, O7 and O18 (7).…”

Virulence potential of a multidrug-resistant Escherichia coli strain belonging to the emerging clonal group ST101-B1 isolated from bloodstream infection

“…Complement resistance confers the possibility to spread to different body sites through the bloodstream. Hallström et al [54] reported the relationship of bacterial resistance to NHS with sepsis severity, and other authors have associated it to different kinds of extraintestinal infections [55–57].…”

Genotypic and phenotypic characteristics of Escherichia coli involved in transfusion‐transmitted bacterial infections: implications for preventive strategies

“…20 For each experiment, a control was performed using inactivated fresh plasma (IFP), with incubation at 55 C for 30 minutes to disrupt the classical and alternative pathways of the complement cascades. 19 Overnight cultures were adjusted to 10 6 CFUs/mL in LB for a final volume of 2 mL. FFP alone (Condition A-100 μL of bacterial culture +100 μL of FFP; Condition B-100 μL bacterial culture + 100 μL of IFP) and FFP + PLT protection solution (SPP+; Condition C-100 μL of bacterial culture + 33 μL of FFP + 67 μL of SPP+; Condition D-100 μL of bacterial culture + 33 μL of IFP + 67 μL of SPP+) were tested.…”

“…Regarding the discrepancy in terms of LT in this environment, we tested three different hypotheses: 20 The control strains, CFT073 and K-12 MG1655, killed 10 of 10 (super killer) and zero of 10 mice in 24 hours (nonkiller), respectively. §S/R = sensitivity or resistance as defined by Hughes et al 19 kSPP+ is a PLT protection solution. Once the serum was heat-inactivated, all of the strains (TTBI and IAI) became resistant to the serum with and without SPP+ (data not shown).…”