ABSTRACT
In December 2000, a female infant hospitalized in our Neonatal Care Centre was infected with varicella by her mother. Although prophylactic intravenous acyclovir was administered at a dose of 15 mg/kg daily, she later developed varicella during her hospital stay. We therefore initiated control procedures to prevent further hospital-acquired infections. Oral acyclovir (40 mg/kg daily divided into four doses) was administered prophylactically to six preterm infants in contact with the varicella patient. None of six preterm infants subsequently developed clinical varicella or had any adverse effects associated with acyclovir administration. It is suggested that prophylactic administration of oral acyclovir (40 mg/kg daily) might prevent hospital-acquired varicella-zoster virus (VZV) infections, and that oral acyclovir may be an option for VZV prophylaxis in situations where VZV immunoglobulin is not available.
Subject(s)
Acyclovir/administration & dosage , Antiviral Agents/administration & dosage , Cross Infection/prevention & control , Environmental Exposure/prevention & control , Herpesviridae Infections/prevention & control , Herpesvirus 3, Human , Intensive Care Units, Neonatal , Administration, Oral , Chemoprevention , Cross Infection/virology , Female , Humans , Infant, NewbornABSTRACT
Many reports have associated intrauterine growth retardation (IUGR) with adverse neurological outcome, but the underlying pathology is imperfectly understood. We have developed a new rat model of IUGR using maternal administration of synthetic thromboxane A(2) (STA(2)). In the present study, the effect of this insult on neuronal migration in the rat cerebral cortex was examined. Bromodeoxyuridine (BrdU), a time-specific cell marker was administered intraperitoneally to the mothers on embryonic day (E) 19. At postnatal day (P) 3, P4, P5, and P6, pups were terminally anesthetized and brains were removed. BrdU-labeled cells were detected immunohistochemically and counted in cerebrum, which was divided into the cortical plate (CP), the intermediate zone, and the subventricular/ventricular zone (SVZ+VZ). Numbers of labeled cells in the three areas over time were compared between IUGR and control animals. Numbers of labeled cells in SVZ+VZ were significantly greater in IUGR than in controls at P3, 5, and 6 (P<0.05). In contrast, labeled cells in the CP were significantly less abundant in IUGR animals than in controls at P3, 4, and 6 (P<0.05). We concluded that neuronal migration was delayed in IUGR rats.
Subject(s)
Brain/pathology , Cell Movement , Disease Models, Animal , Fetal Growth Retardation/chemically induced , Neurons/physiology , Thromboxane A2 , Animals , Animals, Newborn , Female , Fetal Growth Retardation/pathology , Pregnancy , Rats , Rats, Sprague-DawleyABSTRACT
Intrauterine growth retardation (IUGR) often results in clinical neurodevelopmental disorders. To clarify the influence of uteroplacental insufficiency on central nervous system development, we have created a model of IUGR in rats using maternal administration of synthetic thromboxane A(2). We investigated expression patterns of neural cell adhesion molecule (NCAM) and reelin in this model by semiquantitative competitive polymerase chain reactions. On postnatal day 2, NCAM expression was decreased in rat cerebral cortex, and reelin expression was decreased in hippocampus from levels in controls without maternal thromboxane exposure. No significant differences in NCAM expression were seen in hippocampus, nor did reelin expression differ in cerebral cortex between control and IUGR groups. We also examined expression of two neurotrophic factors, brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3). In cerebral cortex the IUGR group showed less BDNF and NT-3 expression than controls. Delay of neuronal migration and histological changes observed in our IUGR rats may be related to altered expression of these molecules.
