The effect of second-generation pneumococcal conjugate vaccines on invasive pneumococcal disease (IPD) strain distributions have not yet been well described. We analysed IPD isolates recovered from children aged <5 years through Active Bacterial Core surveillance before (2008–2009; n = 828) and after (2011–2013; n = 600) 13-valent pneumococcal conjugate vaccine (PCV13) implementation. We employed conventional testing, PCR/electrospray ionization mass spectrometry and whole genome sequence (WGS) analysis to identify serotypes, resistance features, genotypes, and pilus types. PCV13, licensed in February 2010, effectively targeted all major 19A and 7F genotypes, and decreased antimicrobial resistance, primarily owing to removal of the 19A/ST320 complex. The strain complex contributing most to the remaining β-lactam resistance during 2011–2013 was 35B/ST558. Significant emergence of non-vaccine clonal complexes was not evident. Because of the removal of vaccine serotype strains, positivity for one or both pilus types (PI-1 and PI-2) decreased in the post-PCV13 years 2011–2013 relative to 2008–2009 (decreases of 32–55% for PI-1, and >95% for PI-2 and combined PI-1 + PI-2). β-Lactam susceptibility phenotypes correlated consistently with transpeptidase region sequence combinations of the three major penicillin-binding proteins (PBPs) determined through WGS analysis. Other major resistance features were predictable by DNA signatures from WGS analysis. Multilocus sequence data combined with PBP combinations identified progeny, serotype donors and recipient strains in serotype switch events. PCV13 decreased the frequency of all PCV13 serotype clones and concurrently decreased the frequency of strain subsets with resistance and/or adherence features conducive to successful carriage. Our results serve as a reference describing key features of current paediatric IPD strains in the USA after PCV13 implementation.

Background Streptococcus agalactiae (Group B Streptococcus, GBS) is a leading cause of meningitis, sepsis and pneumonia in neonates in the United States. GBS also causes invasive disease in older infants, pregnant women, children and young adults with underlying medical conditions, and older adults. Resistance to lincosamides in the absence of erythromycin resistance is rare in GBS, but has been previously reported in clinical isolates, both on its own or in combination with resistance to streptogramins A and pleuromutilins (L/LSA/LSAP phenotypes). Objectives To retrospectively screen the Active Bacterial Core surveillance (ABCs) GBS isolate collection for these phenotypes in order to identify the causal genetic determinants and determine whether their frequency is increasing. Methods Based on MIC data, 65 (0.31%) isolates susceptible to erythromycin (MIC ≤0.25 mg/L) and non-susceptible to clindamycin (MIC ≥0.5 mg/L) were identified among 21186 GBS isolates. Genomic DNA was extracted and WGS was performed. The presence of 10 genes previously associated with LSA resistance was investigated by read mapping. Results Forty-nine (75%) isolates carried the lsa(C) gene and expressed the LSAP phenotype, and 12 (18%) carried both the lnu(B) and lsa(E) genes and expressed the LSAP phenotype. The four remaining isolates were negative for all determinants investigated. Conclusions While the overall observed frequency of these phenotypes among our GBS isolates was quite low (0.31%), this frequency has increased in recent years. To the best of our knowledge, this is the first time the LSAP phenotype has been reported among GBS isolates from the USA.

Introduction: Falls are the leading cause of traumatic brain injury (TBI) for children in the 0–4 year age group. There is limited literature pertaining to fall-related TBIs in children age 4 and under and the circumstances surrounding these TBIs. This study provides a national estimate and describes actions and products associated with fall-related TBI in this age group. Method: Data analyzed were from the 2001–2013 National Electronic Injury Surveillance System–All Injury Program (NEISS–AIP), a nationally representative sample of emergency departments (ED). Case narratives were coded for actions associated with the fall, and product codes were abstracted to determine fall location and product type. All estimates were weighted. Results: An estimated 139,001 children younger than 5 years were treated annually in EDs for nonfatal, unintentional fall-related TBI injuries (total = 1,807,019 during 2001–2013). Overall, child actions (e.g., running) accounted for the greatest proportion of injuries and actions by others (e.g., carrying) was highest for children younger than 1 year. The majority of falls occurred in the home, and involved surfaces, fixtures, furniture, and baby products. Conclusions: Fall-related TBI in young children represents a significant public health burden. The majority of children seen for TBI assessment in EDs were released to home. Prevention efforts that target parent supervision practices and the home environment are indicated. Practical applications: Professionals in contact with parents of young children can remind them to establish a safe home and be attentive to the environment when carrying young children to prevent falls.

Summary V1aR has a well established role in the neural regulation of adult mammalian social behavior. The role of V1aR in developmentally emerging social behavior is less well understood. We mapped V1aR at post-natal day 8 (P8) and demonstrate developmentally-specific expression in the neocortex and hippocampus. We tested the ability of male and female C57BL/6J mice to show orienting bias to a familiar odor at this age. We demonstrate that females, but not males, show an orienting bias for odors previously paired with the mother, which is eliminated by V1aR signaling. Arginine-vasopressin (AVP) and the vasopressin V1a receptor (V1aR) acting within the forebrain are involved in social behavior in adult animals. Much less is known about the function of V1aR in neurobehavioral development. In the present study, at post-natal day 8 (P8) in neonatal C57BL/6J mice, we map V1aR and use an olfactory exposure paradigm to assess a role for V1aR on olfactory preferences. In addition to V1aR in the lateral septum and ventral tegmental area, we observe V1aR in the neocortex and hippocampus, not typically observed in adult mice, implicating a developmental sensitive period for V1aR to modulate these brain areas in an experience-dependent manner. Males and females were tested on P8 for orienting preferences after exposure to a non-social odor, presented either when the mother was in the home cage (contingent) or when the mother had been removed from the home cage (not contingent). Wild-type female mice show a selective orienting bias toward the exposed odor, but only in the contingent condition. Males did not show orienting bias after either training condition. Female Avpr1a-/- mice showed strong familiar odor bias, regardless of the training condition. This finding led us to test the ability of AVP to diminish odor bias in females. Central application of AVP eliminated odor bias in Avpr1a+/+, but not Avpr1a-/- female mice. Together, these data indicate that AVP acting at V1aR eliminates the expression of familiar odor bias in neonatal mice. This suggests a developmental role for AVP on familiarity bias, which has implications for species-typical life history trajectories of social learning and natal dispersal.