Abstract. Although scrub typhus is uncommon in pregnant women, when present, it can have serious repercussions for the mother and developing fetus. Since it is uncommon, the clinical impact of scrub typhus on pregnancy has not been elucidated and an effective and safe therapeutic regimen has not been validated. The medical records of pregnant women whose scrub typhus were treated at Chungnam National University Hospital were reviewed and their clinical outcomes were evaluated. A review of the literature was also performed on pregnant women with scrub typhus and their clinical outcomes. Eight pregnant women with scrub typhus were treated successfully with a single 500-mg dose of azithromycin, and no relapses were reported. They all delivered healthy babies at term, without congenital or neonatal complications. In the reviews, azithromycin was effective against scrub typhus and had favorable pregnancy outcomes. Ciprofloxacin and cefuroxime failed to treat scrub typhus and fetal loss resulted. A single 500-mg dose of azithromycin may be a reasonable treatment regimen for pregnant women with scrub typhus. Ciprofloxacin might not be advisable for the treatment of scrub typhus during pregnancy. Scrub typhus itself seems to have serious adverse effects on pregnancy if not appropriately controlled.

Neonatal sepsis remains one of the most important causes of death and co-morbidity in very-low-birth-weight (VLBW) infants. The aim of this study was to determine the current incidences of early-onset sepsis (EOS) and late-onset sepsis (LOS), the distribution of pathogens, and the impact of infection on co-morbidities in VLBW infants. We analyzed the data including sepsis episode from 2,386 VLBW infants enrolled in Korean Neonatal Network from January 2013 to June 2014. We defined EOS as a positive blood culture occurring between birth and 7 days of life and LOS after 7 days of life. Sepsis was found in 21.1% of VLBW infants. The risk of sepsis was inversely related to birth weight and gestational age. EOS was found in only 3.6% of VLBW infants, however the mortality rate was as high as 34.1%. EOS was associated with the increased odds for bronchopulmonary dysplasia and intraventricular hemorrhage. The vast majority of EOS was caused by Gram-positive organisms, particularly coagulase-negative staphylococci (30.6%). LOS developed in 19.4% of VLBW infants with a 16.1% mortality rate. Pathogens in LOS were dominated by coagulase-negative staphylococci (38.3%). Twenty-five percent and fifty percent of first LOS episode occurred after 12 days and 20 days from birth, respectively. Younger and smaller VLBW infants showed the earlier occurrence day for the 25% of first LOS episode. This study provides a recent nationwide epidemiology of sepsis in VLBW infants in Korea. Based on this study, successful strategies to reduce infections would improve survival and reduce morbidity.

Background: Neonatal seizures can result in chronic epilepsy and long-term behavioral and cognitive deficits. Levetiracetam (LeV), an antiepileptic drug that binds to the synaptic vesicle protein 2a (sV2a), has been increasingly used off-label for the therapy of neonatal seizures. Preclinical data regarding the acute or long-term efficacy of LeV are lacking. Methods:We tested the anticonvulsant efficacy of LeV in a rat model of hypoxia-induced neonatal seizures. In addition, we evaluated the protective effects of postnatal day (P)10 LeV treatment on later-life kainic acid (Ka)-induced seizure susceptibility and seizure-induced neuronal injury. Western blot and immunohistochemistry were used to assess the developmental regulation of sV2a in the rat and human brain. results: LeV pretreatment at P10 significantly decreased the cumulative duration of behavioral and electrographic seizures at both 25 and 50 mg/kg. at P40, Ka-induced seizures and neuronal loss were significantly diminished in rats previously treated with LeV. LeV target sV2a is present in both neonatal rat and human brain and increases steadily to adulthood. conclusion: LeV suppressed acute seizures induced by perinatal hypoxia and diminished later-life seizure susceptibility and seizure-induced neuronal injury, providing evidence for disease modification. These results support consideration of a clinical trial of LeV in neonatal seizures. n eonatal seizures can be refractory to conventional antiepileptic drugs (AEDs) (1,2), and recently, newer-generation drugs have been considered for off-label use and/or clinical trials for this indication. Levetiracetam ((S)-α-ethyl-2-oxo-1-pyrrolidine acetamide; LEV) is a newer AED with more than a 10-y history of US Food and Drug Administration approval for use as adjunctive therapy for partial epilepsy and is efficacious and safe as monotherapy in adult and pediatric epilepsy syndromes (3,4). LEV has a specific and unique binding target, the synaptic vesicle protein 2A (SV2A), which is involved in exocytosis of synaptic vesicles by interacting with the soluble N-ethylmaleimide-sensitive factor attachment protein receptor complex (5). SV2A is widely expressed throughout all brain structures regardless of the neurotransmitter phenotype (6). LEV binding to SV2A impedes neurotransmitter exocytosis and can block the interaction of the SV2A protein with the actin cytoskeletal network involved in the synaptic vesicle trafficking (7). LEV has also been shown to modulate voltageoperated K + channels (8) and N-type high-voltage-activated Ca 2+ currents (9). Previous studies in adult animal models of chronic epilepsy demonstrate that LEV is a potent anticonvulsant with longlasting antiepileptogenic effects, even as a single dose (10-13). Unlike other conventional AEDs, LEV has no negative impact on cognition and memory formation in either normal or chronically epileptic rats (14). Taken together, these properties and its unique safety profile make LEV an attractive candidate drug for seizure suppression and antiepileptogen...

There is a delicate balance between too little and too much supplemental oxygen exposure in premature infants. Since underuse and overuse of supplemental oxygen can harm premature infants, oxygen saturation levels must be monitored and kept at less than 95% to prevent reactive oxygen species-related diseases, such as retinopathy of prematurity and bronchopulmonary dysplasia. At the same time, desaturation below 80 to 85% must be avoided to prevent adverse consequences, such as cerebral palsy. It is still unclear what range of oxygen saturation is appropriate for premature infants; however, until the results of further studies are available, a reasonable target for pulse oxygen saturation (SpO2) is 90 to 93% with an intermittent review of the correlation between SpO2 and the partial pressure of arterial oxygen tension (PaO2). Because optimal oxygenation depends on individuals at the bedside making ongoing adjustments, each unit must define an optimal target range and set alarm limits according to their own equipment or conditions. All staff must be aware of these values and adjust the concentration of supplemental oxygen frequently.