Differences in the presence of nine urovirulence factors among clinical isolates of Escherichia coli causing cystitis and pyelonephritis in women and prostatitis in men have been studied. Hemolysin and necrotizing factor type 1 occur significantly more frequently among isolates causing prostatitis than among those causing cystitis (P < 0.0001) or pyelonephritis (P < 0.005). Moreover, the papGIII gene occurred more frequently in E. coli isolates associated with prostatitis (27%) than in those associated with pyelonephritis (9%) (P < 0.05). Genes encoding aerobactin and PapC occurred significantly less frequently in isolates causing cystitis than in those causing prostatitis (P < 0.01 and P < 0.0001, respectively) and pyelonephritis (P < 0.01 and P < 0.0001, respectively). No differences in the presence of Sat or type 1 fimbriae were found. Finally, AAFII and Bfp fimbriae are no longer considered uropathogenic virulence factors since they were not found in any of the strains analyzed. Overall, the results showed that clinical isolates producing prostatitis need greater virulence than isolates producing pyelonephritis in women or, in particular, cystitis in women (P < 0.05). Overall, the results suggest that clinical isolates producing prostatitis are more virulent that those producing pyelonephritis or cystitis in women.Urinary tract infections (UTIs) are one of the most common infectious diseases encountered in the clinical practice, mainly being associated with different members of the family Enterobacteriaceae. In fact, Escherichia coli is by far the most predominant pathogen causing UTIs (4,18,19,21).In general, rates of UTIs are higher among women than among men (15), with cystitis being the most prevalent UTI in women. It is noteworthy that the prevalence of quinolone resistance among E. coli strains causing cystitis is significantly higher than the prevalence of quinolone resistance among strains causing urinary parenchymatous infections such as prostatitis and pyelonephritis (2, 23). Velasco et al. (23) found that 20% of the isolates causing cystitis were resistant to ciprofloxacin, while only 8% of the invasive isolates causing UTIs had a resistant phenotype. Some studies suggest that resistance to the quinolones may be associated with a diminished virulence of the uropathogenic strains (16). Moreover, in a recent work (25), the prevalence of different genes encoding certain virulence factors among quinolone-resistant E. coli isolates causing cystitis and pyelonephritis in women was found to be lower than that among quinolone-susceptible strains.Both host and bacterial factors have been associated with the pathogenesis of these infections (9, 21). Thus, uropathogenic strains of E. coli are believed to display a variety of virulence properties that help them colonize host mucosal surfaces and circumvent host defenses to allow invasion of the normally sterile urinary tract (15,18,21). A number of virulence determinants have been related to the acquisition or development of UTIs. Among these factors, sidero...

Quinolone-resistant (QR) Escherichia coli may have lower invasive capacity than does quinolone-susceptible E. coli. To evaluate this, we prospectively collected data regarding all cases of E. coli invasive urinary tract infections (IUTI) in 669 adults admitted to the Infectious Diseases Unit of our hospital during a 3-year period, as well as 10,950 patients with cystitis or asymptomatic bacteriuria who presented to the outpatient clinic during a 1-year period. QR E. coli was isolated in 20% of patients with cystitis, compared with 8% of those with IUTI (P<.05). The proportion of E. coli isolates that were quinolone resistant was similar in patients with bacteremic and nonbacteremic IUTI. The factors of urinary manipulation and structural abnormalities were independently associated with the presence of quinolone resistance. Old age was the only variable independently associated with blood invasion. QR E. coli is less likely to produce invasive disease (pyelonephritis and prostatitis) than is quinolone-susceptible E. coli. However, once pyelonephritis or prostatitis have developed, there is no difference in the incidence of bacteremia.

The aim of the study is to evaluate demographics, epidemiology, clinical characteristics, treatment and outcomes of Clostridium difficile infection (CDI) in patients with and without concurrent cancer. This is a prospective cohort study of consecutive primary CDI episodes in adults (January 2006-December 2016). CDI was diagnosed on the presence of diarrhoea and positive stool testing for toxigenic C. difficile. Univariate analysis assessed differences between cancer and non-cancer patients. Risk factors of all-cause 30-day mortality were determinate using the logistic multivariable procedure. In total, 787 CDI episodes were recorded, 191 in cancer patients (median age 64, IQR 50-73). Of these, 120 (63%) had solid and 71 (37%) haematological malignancies (24 received a stem cell transplant). At the CDI diagnosis, 158 (82.7%) cancer patients had prior antibiotics and 150 (78.5%) were receiving proton pump inhibitors. Fifty-seven (80.3%) patients with haematological and 52 (43.3%) with solid malignancies were under chemotherapy at diagnosis; 25 (35.2%) with haematological and 11 (9.2%) with solid malignancies had an absolute neutrophil count < 1000/mm. Overall, 30-day mortality was higher in cancer patients than in those without (19.2 vs. 8.6% respectively, p < 0.001); recurrence rates did not vary significantly (11.1 vs. 11%, p = 0.936). By type of neoplasm, 30-day mortality was higher in patients with haematological malignancies and solid tumours than in patients without cancer (respectively, 25.4 vs. 8.6%; p < 0.001 and 15 vs. 8.6%; p < 0.001). Our results suggest that the prognosis of CDI (30-day mortality) is poorer in patients with cancer than in those without although percentages of recurrent infection are similar in these two patient populations.

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