Background The ferroxidase zyklopen (Zp) has been implicated in the placental transfer of iron to the fetus. However, the evidence for this is largely circumstantial. Objectives This study aimed to determine whether Zp is essential for placental iron transfer. Methods A model was established using 8- to 12-wk-old pregnant C57BL/6 mice on standard rodent chow in which Zp was knocked out in the fetus and fetal components of the placenta. Zp was also disrupted in the entire placenta using global Zp knockout mice. Inductively coupled plasma MS was used to measure total fetal iron, an indicator of the amount of iron transferred by the placenta to the fetus, at embryonic day 18.5 of gestation. Iron transporter expression in the placenta was measured by Western blotting, and the expression of Hamp1, the gene encoding the iron regulatory hormone hepcidin, was determined in fetal liver by real-time PCR. Results There was no change in the amount of iron transferred to the fetus when Zp was disrupted in either the fetal component of the placenta or the entire placenta. No compensatory changes in the expression of the iron transport proteins transferrin receptor 1 or ferroportin were observed, nor was there any change in fetal liver Hamp1 mRNA. Hephl1, the gene encoding Zp, was expressed mainly in the maternal decidua of the placenta and not in the nutrient-transporting syncytiotrophoblast. Disruption of Zp in the whole placenta resulted in a 26% increase in placental size (P < 0.01). Conclusions Our data indicate that Zp is not essential for the efficient transfer of iron to the fetus in mice and is localized predominantly in the maternal decidua. The increase in placental size observed when Zp is knocked out in the entire placenta suggests that this protein may play a role in placental development.

BackgroundGroup B streptococcal infections (GBSs) in nonpregnant adults have become an increasingly recognized entity. Bacteremia without focus has consistently been demonstrated as the second leading cause of infection. Recurrent bacteremia, however, remains a significantly rarer phenomenon, and underlying mechanisms and risk factors are poorly elucidated in the literature.Case ReportWe report the first case of 3 independent episodes Streptococcus agalactiae bacteremia without focus, in 56-year-old woman with Child-Pugh B cirrhosis and the uncommon finding of portal hypertensive colopathy.ResultsWe propose bowel hemorrhage secondary to portal hypertensive colopathy, facilitated recurrent bacterial translocation and blood stream infection in this immunocompromised host, presenting as recurrent bacteremia without focus. We discuss the disease epidemiology of GBS infections, antibiotic sensitivity, and risk factors for infection relating to this theory in a literature review.ConclusionsPortal hypertensive colopathy in liver cirrhosis may contribute to underlying risk for recurrent GBS bacteremia without focus that necessitates prolonged penicillin class antibiotic therapy.