The effect of obstetric practice change to reduce early term delivery on perinatal outcome.

OBJECTIVE: To investigate whether the national emphasis on attaining 39 weeks gestation has altered obstetric practice, and if so whether this has affected perinatal morbidity. STUDY DESIGN: We examined trends in gestational age, neonatal morbidity, maternal complications and stillbirth for a retrospective cohort of singleton, live births between 37+0 and 39+6 weeks of gestation over a 5-year period at a single tertiary care center. RESULT: There were 21 343 eligible deliveries. The proportion of deliveries in the early term (<39 weeks) decreased from 47.8 to 40.2% (P<0.01). The reduction was most pronounced for elective inductions (27.5 to 8.0%; P<0.01) and scheduled cesareans (56.9 to 24.9%; P<0.01), although a similar trend was seen for nonelective inductions (51.2 to 47.9%; P=0.03). In multivariable analysis, there was a 10% decreased odds of early term delivery per year (P<0.01). There were no changes in the rates of neonatal intensive care unit (NICU) evaluation (29.8 to 28.1%; P=0.11), pre-eclampsia (7.6 to 8.5%; P=0.06) or stillbirth (11.5 to 14.4 per 10 000; P=0.55). CONCLUSION: A 10% annual decline in the odds of early term delivery was not accompanied by significant changes in perinatal morbidity.

Neonatal early-onset sepsis evaluations among well-appearing infants: projected impact of changes in CDC GBS guidelines.

OBJECTIVE: To determine (a) the proportion of asymptomatic infants born at ≥35 weeks gestation evaluated for early-onset sepsis (EOS) and exposed to postnatal antibiotics; (b) reasons for and outcomes of the evaluations, and (c) anticipated changes when applying the Centers for Disease Control and Prevention (CDC) 2010 guidelines to this study population. STUDY DESIGN: Retrospective cohort study of infants born at ≥35 weeks gestation in 2008-2009 in a large maternity center. RESULT: Out of the 7226 infants that met the study criteria: 1062 (14.7%) were evaluated for EOS and half of those evaluated, received empiric antibiotics. 70.4% of evaluations were performed owing to maternal intrapartum fever, but 23% were prompted by inadequate Group B Streptococcus (GBS) prophylaxis alone. Three cases of blood culture-proven infection were identified. CONCLUSION: Improved approaches are needed to identify asymptomatic infants who are at risk for EOS to decrease unnecessary evaluations and antibiotic exposure. Transition to the 2010 CDC GBS guidelines may eliminate a quarter of EOS evaluations among these infants.

Tandem repeat deletion in the alpha C protein of group B streptococcus is recA independent.

Group B streptococci (GBS) contain a family of protective surface proteins characterized by variable numbers of repeating units within the proteins. The prototype alpha C protein of GBS from the type Ia/C strain A909 contains a series of nine identical 246-bp tandem repeat units. We have previously shown that deletions in the tandem repeat region of the alpha C protein affect both the immunogenicity and protective efficacy of the protein in animal models, and these deletions may serve as a virulence mechanism in GBS. The molecular mechanism of tandem repeat deletion is unknown. To determine whether RecA-mediated homologous recombination is involved in this process, we identified, cloned, and sequenced the recA gene homologue from GBS. A strain of GBS with recA deleted, A909DeltarecA, was constructed by insertional inactivation in the recA locus. A909DeltarecA demonstrated significant sensitivity to UV light, and the 50% lethal dose of the mutant strain in a mouse intraperitoneal model of sepsis was 20-fold higher than that of the parent strain. The spontaneous rate of tandem repeat deletion in the alpha C protein in vitro, as well as in our mouse model of immune infection, was studied using A909DeltarecA. We report that tandem repeat deletion in the alpha C protein does occur in the absence of a functional recA gene both in vitro and in vivo, indicating that tandem repeat deletion in GBS occurs by a recA-independent recombinatorial pathway.