The transmission of maternal E. coli colonizing the newborn can occur after colonization

or infection of amniotic fluid, after membrane rupture or on passage of the neonate through the vaginal canal during delivery, and may cause early neonatal infection. Data on the features and virulence factors of infection-causing E. coli strains in mothers and babies, and colonization of genital tracts of pregnant women by this microorganism are scarce. Neonatal sepsis by E. coli is related to a limited number of phylogenetic groups B2 and D, both considered as virulent. The pathogenicity of these groups is associated with the presence of several virulence factors, some of which are contained into pathogenicity islands (PAIs) (Soto Galunisertib chemical structure et al., 2008). The study of these E. coli strains is necessary to understand the potential risk factors for vertical transmission of neonatal infection by pregnant women and to design interventions selleck products to address such risk factors adequately. The aim of this study was to compare the virulence factors present in E. coli isolates from the genital tract of pregnant women with those of E. coli from nonpregnant women in order to shed light on the possible differences in the virulence profiles that could

explain their capacity to cause severe infections. The study included 648 vaginal and endocervical samples from 321 pregnant and 327 nonpregnant women followed either at the antenatal visits or at the Gynecology Department of the Hospital Clinic of Barcelona. Samples from each woman were collected using sterile swabs. The samples were spread in chocolate agar (PVX, BioMèrieux, Spain). Colonies with an E. coli appearance were grown in McConkey agar (MCK, BioMèrieux) with subsequent biochemical

identification using the β-glucuronidase/indol test (DIATABS, Rosco Diagnostica, Taastrup). Escherichia coli isolates P-type ATPase were grown in blood agar plates (COS, Oxoid) to study their hemolytical capacity. The virulence profile was analyzed by PCR using gene-specific primers for 17 virulence genes such as hemolysin (hly), cytotoxic necrotizing factor (cnf1), autotransporter (sat1), P-fimbriae (pap genes), type 1C fimbriae (focG), yersiniabactin (fyu), heat-resistant hemagglutinin (hra), S-fimbriae (sfaS), invasin (ibeA), adhesin (iha), aerobactin (iucD), siderophores (iutA, iroN) and antigen 43 (ag43) (Table 1). PCR conditions were 94 °C for 4 min, followed by 30 cycles of 94 °C for 30 s, the corresponding annealing temperature (55–63 °C) for 30 s, 72 °C for 2 min and a final elongation of 72 °C for 5 min. Samples were run in 1.5% agarose gels and stained with SYBR Safe DNA gel stain (Invitrogen, Spain). The E.