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9 Group B Streptococcus Meningitis 9 Group B Streptococcus Meningitis Victor Nizet1 and Kelly S. Doran1,2* 1University of California at San Diego, California, USA; 2San Diego State University, San Diego, USA 9.1 Introduction infections are traditionally divided among two forms: early-onset disease (EoD) and Streptococcus agalactiae (Group B Streptococcus, late-onset disease (LoD). Early-onset in- GBS) is a Gram-positive encapsulated fections are described to occur through the bacterium possessing an array of virulence fi rst 7 days of life, but in fact have a median factors that render it capable of producing onset of only 6–8 h of life, presenting acutely serious disease in susceptible hosts, in with pneumonia and respiratory failure particular the human newborn (Maisey et al., complicated by bloodstream infection and 2008a). Notably, GBS is the leading cause of septicaemia. GBS EoD cases result from meningitis in the neonatal period (Brouwer et ascending infection of the bacterium through al., 2010; Thigpen et al., 2011). Although the placental membranes to initiate infection advances in intensive care management and in utero, or, alternatively, by aspiration of antibiotic therapy have changed GBS infected vaginal fl uids during the birth meningitis from a uniformly fatal disease to a process. Premature, low-birth-weight infants frequently curable one, the overall outcome are at increased risk of developing early- remains unfavourable. Morbidity is high; onset infection, with GBS placental infection 25–50% of surviving infants suff er neuro- itself oft en the critical factor triggering logical sequelae of varying severity, including premature labour. In contrast, GBS LoD cerebral palsy, mental retardation, blindness, occurs in infants up to 7 months of age, with deafness or seizures. more indolent symptom progression related The pathogenesis of neonatal GBS to bacteraemia, absence of lung involvement infection begins with the asymptomatic and a high incidence (~50%) of meningitis colonization of the female genital tract. (Baker and Edwards, 2001). Universal Approximately 20–30% of healthy women screening of pregnant women at 35–37 weeks are colonized with GBS on their vaginal or gestation and intrapartum antibiotic rectal mucosa, and 50–70% of infants born to prophylaxis has resulted in a decline in early- these women will themselves become onset GBS invasive disease in the USA (Phares colonized with the bacterium (Baker and et al., 2008; Van Dyke et al., 2009). However, Edwards, 2001). For the purposes of this treatment has not eliminated the epidemiological classifi cation, neonatal GBS incidence of GBS meningitis, and concern has *[email protected] © CAB International 2013. Meningitis: Cellular and Molecular Basis 118 (ed. M. Christodoulides) Group B Streptococcus Meningitis 119 been raised about concurrent increases in fl uid barrier (BCSFB). For the purposes of this non-GBS early-onset bacterial infections, review, the BBB and BCSFB are inter- especially in pre-term infants as a result of changeable concepts with respect to vessel increased antibiotic use (Stoll et al., 2002a,b). endothelial cell penetration by GBS. Furthermore, the occurrence of GBS Disruption of BBB integrity is a hallmark meningitis in older children or adults is more event in the pathophysiology of bacterial commonly appreciated, with an approximate meningitis. This disruption may be due to the 4% increase in total number of cases reported combined eff ect of bacterial entry and between 1997 and 2007 in the USA (Thigpen penetration of brain microvascular endo- et al., 2011). No vaccination strategies are thelial cells (BMECs), direct cellular injury by currently in place to prevent GBS infections, bacterial cytotoxins, and/or activation of host but if ultimately achieved they would be infl ammatory pathways that compromise anticipated to reduce the number of BMEC barrier function. It is apparent that the meningitis cases (Thigpen et al., 2011). Here host immune response is not only incapable we review the current understanding of the of controlling infection within the CNS but pathogenesis of GBS meningitis, highlighting also may be responsible for many adverse important bacterial virulence factors and host events during bacterial meningitis (Tunkel interactions that promote disease progression. and Scheld, 1995). A very complex and integrated series of events involving host cytokines, chemokines, proteolytic enzymes 9.2 Pathophysiology of GBS and oxidants appears to be responsible for Meningitis meningitis-induced brain dysfunction. The development of GBS meningitis progresses The pathophysiology of GBS meningitis through phases including: (i) bloodstream varies according to age of onset. In EoD, survival and the development of bacteraemia; autopsy studies demonstrate litt le or no (ii) direct GBS invasion and disruption of the evidence of leptomeningeal infl ammation, BBB/BCSFB; and (iii) GBS multiplication in despite the presence of abundant bacteria, the CSF-containing subarachnoid and ven- vascular thrombosis and parenchymal tricular spaces, which induces infl ammation haemorrhage (Quirante et al., 1974). By with associated pathophysiological alter- contrast, infants with LoD usually have dif- ations leading to the development of neural fuse purulent arachnoiditis with prominent damage. Brain injury results mainly from involvement of the base of the brain (Berman cerebrovascular involvement leading to and Banker, 1966). Similar age-related cerebral ischaemia, brain oedema, hydro- diff erences in central nervous system (CNS) cephalus and increased ICP. pathology are evident in the infant rat model of invasive disease (Ferrieri et al., 1980). These histopathological diff erences refl ect under- 9.2.1 Bloodstream survival and the development of the host immunological development of bacteraemia response in the immediate neonatal period, with a higher proportion of deaths resulting An association between sustained high-level from overwhelming septicaemia. Clinical and bacteraemia and the development of GBS neuropathological studies have documented meningitis has been suggested in humans and the clear association between bacterial in experimental models of haemato geneous meningitis and brain oedema formation, meningitis (Ferrieri et al., 1980; Doran et al., increased intracranial pressure (ICP), seizure 2002a). This observation implies that GBS activity, arterial and venous cerebral vascular bloodstream survival is an important insults, and other neurological sequelae virulence trait to avoid immune clearance by (Scheld et al., 2002). phagocytic killing by host immune cells, prior To produce meningitis, blood-borne GBS to CNS penetration. Neonates are particularly must typically penetrate the blood–brain prone to invasive disease because of their barrier (BBB) and/or the blood–cerebrospinal quantitative or qualitative defi ciencies in 120 V. Nizet and K.S. Doran phagocytic cell function, specifi c antibody, or 2007). The β-antigen of C protein binds human the classical and alternative complement IgA antibody (Jerlstrom et al., 1991), and non- pathways. In addition to these newborn host specifi c deposition of IgA on the bacterial susceptibilities, GBS possess a number of surface probably inhibits inter actions with virulence determinants that promote blood- complement. Finally, a cell-surface protease, stream survival by thwarting key components CspA, targets host fi brinogen, producing of eff ective opsonophagocytic killing such as adherent fi brin-like cleavage products that complement (Fig. 9.1). For example, the coat the bacterial surface and interfere with surface-anchored GBS β-protein prevents complement-mediated opsonophagocytic opsonophagocytosis by binding short clearance (Harris et al., 2003). consensus repeats found in the middle region The profi le of GBS gene transcription of factor H, a host counter-regulator of changes dramatically during growth in complement (Maruvada et al., 2008), enabling human blood, resulting in an altered cell the unbound active region to block C3b morphology and increased expression of deposition on the bacterial cell surface (Jarva complement regulatory proteins (Santi et al., et al., 2004). In addition, the cell-surface GBS 2007; Mereghett i et al., 2008). The sialylated immunogenic bacterial adhesin (BibA) binds GBS capsular polysaccharide (CPS) represents human C3bp, promoting resistance to one of the most critical factors for limiting the phagocytic killing and contributing to eff ectiveness of host complement and virulence in the mouse model (Santi et al., phagocytic defence. Passage of GBS in animals Interference with C3 complement function Phagocyte lysis and apoptosis Factor H C3 Fibrinogen C3bp β-protein CspA BibA H2O2 Fibrin-like – O2 fragments Antioxidant GBS defence C3 pigment SOD Sialic acid in polysaccharide Capsule β-haemolysin/ cytolysin Bind/sequester Charge repulsion PBP1a (pilus subunit PilB) (Dlt operon) Antimicrobial peptide resistance Fig. 9.1. Mechanisms of GBS immune evasion. GBS express multiple surface-exposed or secreted factors to evade host immune defences and promote bloodstream survival. The PBP1a and the PilB subunit of GBS pili contribute to antimicrobial peptide resistance. The Dlt operon is responsible for increasing incorporation of D-alanine residues in cell-wall teichoic acids, thereby reducing electronegativity and affi nity for cationic antimicrobial peptides. ScpB, the sialic acid capsule, BibA, -protein and CspA all inhibit host clearance of GBS by interfering with complement components C5a, C3 and C3bp. Superoxide
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