Maternal high-dose valacyclovir and its correlation with newborn blood viral load and outcome in congenital cytomegalovirus infection.

BACKGROUND/OBJECTIVE: Currently, there is no validated treatment for fetal cytomegalovirus (CMV). Two studies suggest that high-dose maternal valacyclovir decreases fetal viral load and improves outcomes in moderately-symptomatic fetuses. We offered valacyclovir in cases of fetal infection lacking ultrasound abnormalities or with non-severe infection. Maternal tolerability, fetal outcome and newborn blood viral load were evaluated in pregnancies of mothers receiving valacyclovir. STUDY DESIGN: We performed a case series including 8 pregnancies with fetal CMV classified as unaffected/mildly-moderately affected. Mothers received valacyclovir (8 g/24h) from fetal infection diagnosis to delivery. Standard newborn evaluation was performed, and viremia was determined in the first 48 h of life and compared according to length of maternal treatment and presence/absence of prenatal anomalies. RESULTS: Valacyclovir was administered at a median gestational age of 26.5 weeks (23.8-33.1) in 3 cases without fetal abnormalities, and 5 with mild/moderate abnormalities. Three were 3 first trimester primary infections, one non-primary infection, and in 4 the type of infection was unknown. Valacyclovir was well-tolerated. Fetal features did not progress. Three newborns were asymptomatic, and one was severely affected (bilateral chorioretinitis). The median newborn viral load (IQR) was 502 IU/mL (231-191781) with lower levels when maternal treatment was administered ≥10 weeks, and in cases without fetal abnormalities [median 234 IU/mL (228-711) vs. 4061 (292-510500) p = .18; and 234 IU/mL (228-379500) vs. 711 IU/mL (292-4061) p = .65, respectively], these differences being non-significant. CONCLUSIONS: Fetal CMV lesions remained stable with high-dose maternal valacyclovir. Newborn viral load was unchanged despite treatment duration and fetal/neonatal abnormalities. SUMMARY: Fetal cytomegalovirus lesions remained stable with high-dose maternal valacyclovir. Newborn viral load was unchanged despite treatment duration and fetal/newborn abnormalities.

Outbreak Caused by Escherichia coli O18: K1: H7 Sequence Type 95 in a Neonatal Intensive Care Unit in Barcelona, Spain.

BACKGROUND: Escherichia coli is one of the most frequent causes of late-onset neonatal sepsis. The aim of this study was to characterize an outbreak of neonatal sepsis occurring in the neonatal intensive care unit of the Hospital Clinic of Barcelona from April to August 2013. METHODS: After presentation of the index case, all E. coli isolates from previously hospitalized neonates, health-care workers and neonates admitted to the neonatal intensive care unit from April to October 2013 were tested for K1 antigen positivity and epidemiologically compared by pulse-field gel electrophoresis. Furthermore, the E. coli K1 strains collected from neonates during this period were analyzed by different methods (serotyping, phylotyping, polymerase chain reaction of virulence factors, antimicrobial resistance and "in vitro" assays in Human Brain Microvascular Endothelial Cells (HBMEC)). RESULTS: An E. coli O18:K1:H7 sequence type 95 and phylogenetic group B2 strain was the cause of the outbreak involving 6 preterm neonates: 1 with late septicemia because of a urinary focus and 5 with late-onset septicemia and meningitis, 3 of whom died. All showed the same pulsotype, full resistance to ampicillin and intermediate resistance to gentamicin. The outbreak strain carried the pathogenicity island (PAI) IIJ96-like domain that could explain the high-grade bacteremia necessary to develop meningitis. CONCLUSIONS: All the E. coli isolates responsible for this outbreak belonged to a single clone suggesting a common source of infection, and it was categorized as O18:K1:H7. Despite the bacteria's pathogenicity has an important role in the severity of infection, the host-associated factors were crucial for the fatal outcomes.