There has been much speculation on the pathogenesis of group B streptococcal disease in the neonate. One of the most likely pathogenic mechanisms is
The incidence of group B streptococcal disease (GBS) is 1-3 cases per 1000 births. Neonates acquire the disease during birth from mothers who harbor the organism. Risk factors include prematurity, premature rupture of membranes, and group B streptococcal carriage. The Gram's stain of cerebrospinal fluid is a rapid test for GBS disease. Although sensitive, the Gram's stain requires experience to differentiate these streptococci from other Gram-positive cocci. Latex tests for GBS antigen are also available, but sensitivity in CSF is not significantly higher than the Gram's stain. GBS can be reduced by intrapartum administration of penicillin. Experimentally, GBS polysaccharide vaccines have also been used. Screening pregnant females early in pregnancy probably offers little advantage because of the possible acquisition of GBS late in the pregnancy. There has been speculation concerning the pathogenesis of GBS. These include failure to activate complement pathways and immobilization of polymorphonuclear leukocytes (PMNs) due to the inactivation of complement C5a, a potent chemoattractant. While GBS is relatively more resistant to penicillin than group A streptococci, the great majority of GBS isolates are still penicillin-susceptible. An aminoglycoside such as gentamicin may be added to GBS treatment regimens due to the relative reduced susceptibility of some strains.
Complement C5a, a potent chemoattractant, activates PMNs
The streptococci are resistant to penicillin
The alternative complement pathway is activated
In the absence of specific antibody, opsonization, phagocyte recognition, and killing do not proceed normally
Bacteria