Quinolone-Resistant Uropathogenic Escherichia coli Strains from Phylogenetic Group B2 Have Fewer Virulence Factors than Their Susceptible Counterparts

Abstract

The prevalence of 31 virulence factors was analyzed among nalidixic acid-susceptible and -resistant Escherichia coli strains from phylogenetic group B2. Hemolysin, cytotoxic necrotizing factor 1, and S and F1C fimbriae genes were less prevalent among nalidixic acid-resistant E. coli strains. Quinolone resistance may be associated with a decrease in the presence of some virulence factors.Extraintestinal pathogenic Escherichia coli (ExPEC) strains have multiple virulence factors (VFs) that confer the potential for pathogenicity (6). Recently, extended virulence genotypes have been reported for ExPEC isolates from patients with diverse extraintestinal syndromes (9). E. coli strains derive from different phylogenetic groups (5). Pathogenic E. coli strains derive mainly from the more virulent phylogenetic group B2 (3,7,13).Recent data suggest that quinolone-resistant ExPEC are less able to cause upper urinary tract infection and have fewer VFs than quinolone-susceptible E. coli (14,15). Some studies have related quinolone resistance and low virulence with phylogenetic origin (8). However, in vitro studies (unpublished data) suggest a decreased pathogenicity of E. coli associated with the acquisition of quinolone resistance itself. To study whether the absence of VFs is associated with resistance specifically within phylogenetic group B2, we investigated the prevalence of 31 VFs among quinolone-resistant versus quinolone-susceptible E. coli urinary tract infection (UTI) isolates, all belonging to phylogenetic group B2 (the most virulent; not intrinsically related to quinolone resistance, as shown for phylogenetic group A) (10). The prevalence of the studied VFs according to susceptibility to ampicillin, cotrimoxazole, and gentamicin was also assessed.E. coli strains isolated from urine from patients with acute pyelonephritis, acute cystitis, or acute prostatitis who presented at our department were identified by conventional biochemical tests. Cystitis, acute pyelonephritis, and acute prostatitis were defined as they were defined previously elsewhere (12). Fifty-three E. coli isolates causing acute pyelonephritis in women, 19 causing cystitis in women, and 13 causing prostatitis in men were analyzed.Susceptibilities to nalidixic acid, ciprofloxacin, ampicillin, cotrimoxazole, and gentamicin were tested by the E-test method (AB Biodisk, Sölna, Sweden). All isolates were assigned to phylogenetic group B2 with the use of the multiplex PCR-based method (1), and all isolates belonged to different clones by Rep-PCR. Extended virulence genotypes, including 31 individual VFs and papA alleles, were determined by multiplex PCR assays and dot blot hybridization, as previously described (7). In addition, sat (secreted autotransporter toxin) was detected using previously described PCR conditions and primers (15). Each isolate was tested in duplicate, in parallel with appropriate positive and negative controls.Statistical analyses were performed by using Fisher's exact and chi-square tests. Stratified analysis was performed by mean...

Association between virulence profile and fluoroquinolone resistance in Escherichia coli isolated from dogs and cats in China

“…Overall, the majority of the virulence genes tested were more prevalent in fluoroquinolone-susceptible isolates than in their resistant counterparts, with the exception of ireA and iutA, which is consistent with a previous study that reported that ireA and iutA were significantly more prevalent in fluoroquinolone-resistant isolates [10]. Additionally, all investigated virulence genes were more prevalent in pathogenic isolates than in commensal isolates, consistent with previous studies [2,31].…”

“…Moreover, previous data also suggested that fluoroquinolone-resistant ExPEC isolates harbored fewer virulence genes than did fluoroquinolone-susceptible isolates from humans [10,11].…”

Studies on avian pathogenic Escherichia coli in commercial broiler chicken in South East Queensland

“…Similar findings have occurred in earlier studies in other parts of the world where low prevalence of VGs were detected among FQ resistant CEC isolates (Horcajada et al, 2005;Huang et al, 2009;Kawamura-Sato et al, 2010). These isolates may have been opportunistic pathogens that acquired FQ resistance (Drews et al, 2005;Vila et al, 2002) or they may be CEC isolates that lost their VGs after they developed mutations in the QRDR (Horcajada et al, 2005;Moreno et al;Sawma-Aouad et al, 2009). Furthermore, the virulence profile of the AmpC harbouring E. coli isolates also varied.…”

“…Only three isolates harboured the IncA/C plasmid, they did not exhibit multidrug or ESC resistance, but there is a potential for acquired resistance as the plasmid is in the population of E. coli on the farms. (Horcajada et al, 2005;Huang et al, 2009;Kawamura-Sato et al, 2010). These isolates may have been opportunistic pathogens that acquired FQ resistance (Drews et al, 2005;Vila et al, 2002) or they may be CEC isolates that lost their VGs after they developed mutations in the quinolone resistance-determining region (QRDR) (Horcajada et al, 2005;Moreno et al, 2006;Sawma-Aouad et al, 2009 This might be part of a much larger study, which may explore the distribution of AmpC β-lactamase genes in avian E. coli isolates at different geographical locations and how similar Australian isolates are to overseas strains.…”

Antibiotic Resistance in Extra Intestinal Pathogenic Escherichia Coli

“…In addition, multi-resistance, defined as resistance to norfloxacin in addition to two or three other antibiotics, has also increased [3,4]. Several reports have indicated that quinolone resistance in uropathogenic E. coli is associated with decreased prevalence or expression of virulence factors compared to quinolonesusceptible strains [5,6]. Vila suggested that a possible reason for this is that virulence genes could be lost concomitant with a mutation at codon 83 of the gyrA gene, which affects super coiling of DNA, leading to changes in gene expression.…”