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Indeed, the serotype distribution in EOD cases was superimposable on that found in pregnant women, corroborating the hypothesis of a vertical transmission (R Creti et?al., unpublished data). CC-19 seems likely to cause invasive diseases among both neonates and adults Fluconazole [4,23,25]. In the present study, the clone identified by the string ��III, rib, PFGE type 3, CC-17�� was the most prevalent and responsible for 18 out of the 20 cases of EOD (90%, p?selleck inhibitor surface-anchored protein (HvgA) that enhances GBS adherence and translocation across the intestinal epithelium and the blood-brain barrier [26]. One EOD case was caused by a serotype IV GBS. Both of the patient��s parents were of Caucasian origin. The same indistinguishable strain was isolated from the mother��s vaginorectal swab. This serotype has seldom been found as a cause of neonatal infections [4,8,27,28] but it predominates in colonized pregnant women in the United Arab Emirates and its incidence of carriage is increasing in the US, suggesting that this www.selleckchem.com/products/Paclitaxel(Taxol).html serotype has the potential to emerge as a neonatal pathogen [24]. A total of nine macrolide-resistant GBS strains (12%) were found. Even if not alarmingly high, this rate stresses the importance of testing GBS isolates from prenatal screening for susceptibility to clindamycin and erythromycin, used as a second choice for intrapartum antibiotic prophylaxis in the case of patients at high risk for anaphylaxis. All erythromycin-resistant isolates but one exhibited one of the resistance genotypes studied, with four isolates harbouring the erm(B) gene, two isolates carrying the mef(E) gene, one isolate possessing the erm(A) gene, and one isolate carrying both erm(B) and mef(E) genes. The erythromycin resistance prevalence was slightly lower than that observed in our previous study on GBS strains from different sources of isolation (16.5%), where it was mostly due to serotype V strains belonging to CC-1 and possessing the erm(B) gene. Serotype V has emerged recently as a cause of human disease with a high propensity to acquire macrolide resistance and to spread throughout the population [8,14,25].