9 Group B Streptococcus Meningitis

9.1 Introduction Streptococcus agalactiae (Group B Streptococcus, GBS) is a Gram-positive encapsulated bacterium possessing an array of virulence factors that render it capable of producing serious disease in susceptible hosts, in particular the human newborn (Maisey et al., 2008a). Notably, GBS is the leading cause of meningitis in the neonatal period (Brouwer et al., 2010; Thigpen et al., 2011). Although advances in intensive care management and antibiotic therapy have changed GBS meningitis from a uniformly fatal disease to a frequently curable one, the overall outcome remains unfavourable. Morbidity is high; 25–50% of surviving infants suff er neuro-logical sequelae of varying severity, including cerebral palsy, mental retardation, blindness, deafness or seizures. The pathogenesis of neonatal GBS infection begins with the asymptomatic colonization of the female genital tract. Approximately 20–30% of healthy women are colonized with GBS on their vaginal or rectal mucosa, and 50–70% of infants born to these women will themselves become colonized with the bacterium (Baker and Edwards, 2001). For the purposes of epidemiological classifi cation, neonatal GBS infections are traditionally divided among two forms: early-onset disease (EoD) and late-onset disease (LoD). Early-onset infections are described to occur through the fi rst 7 days of life, but in fact have a median onset of only 6–8 h of life, presenting acutely with pneumonia and respiratory failure complicated by bloodstream infection and septicaemia. GBS EoD cases result from ascending infection of the bacterium through the placental membranes to initiate infection in utero, or, alternatively, by aspiration of infected vaginal fl uids during the birth process. Premature, low-birth-weight infants are at increased risk of developing early-onset infection, with GBS placental infection itself oft en the critical factor triggering premature labour. In contrast, GBS LoD occurs in infants up to 7 months of age, with more indolent symptom progression related to bacteraemia, absence of lung involvement and a high incidence (~50%) of meningitis (Baker and Edwards, 2001). Universal screening of pregnant women at 35–37 weeks gestation and intrapartum antibiotic prophylaxis has resulted in a decline in early-onset GBS invasive disease in the USA (Phares et al., 2008; Van Dyke et al., 2009). However, this treatment has not eliminated the incidence of GBS meningitis, and concern has