RESUMEN
Uropathogenic strains of Escherichia coli [UPEC] cause the vast majority of urinary tract infections [UTI] in both community and hospital settings. They exhibit a variety of virulence properties that determine the severity of infection. The aim of this study was to determine the prevalence of two urovirulent genes [papC and cnf1] and production of haemolysin among UPEC strains causing community acquired [CA] and hospital acquired [HA] UTI, to test the susceptibility of these strains to different antimicrobial agents and to screen for extended spectrum beta-lactamase [ESBL] production. One hundred UPEC strains were collected during the period from June 2005 to May 2006 from cases of CA [50 strains] and HA [50 strains] UTI. Of them, 40 strains were isolated from upper UTI cases, and 60 strains were isolated from lower UTI cases. PapC and cnf1 genes were detected by real-time TaqMan PCR assay. Haemolysin production was detected phenotypically. The double disk synergy method was used to screen ESBL production. Fifty strains [50%] possessed one or more of the studied virulence factors. They were significantly more frequent among isolates causing upper UTI [75%] than those causing lower UTI [33.33%, X[2] =6.404, p= 0.011], but, no significant difference was found between CA and HA strains. HA-UPEC strains showed significant higher resistance to third and fourth generation cephalosporins, quinolones, and nitrofurantoin. No resistance to carbapenems was detected among our strains. Quinolone resistance was detected in 52% of the strains, with significant prevalence among lower UTI and HA strains. Forty two strains [42%] were multidrug resistant [MDR], with more significant prevalence among HA strains. Both quinolone resistant and MDR isolates exhibited significantly lower virulence score than did the susceptible isolates. Twenty eight strains [28%] were found to be ESBL producers, 79% of them [22/28] were quinolone resistant with no significant differences regarding their source. None of the ESBL producers possessed any of the studied virulence genes. Overall, the results showed that virulence factors were more prevalent among isolates causing upper UTI. Quinolone resistance itself may be a virulence factor in lower UTI with an observed association between it and ESBL production. Further studies are needed to clarify these relations