Streptococcus and Early-Onset Sepsis in the Era ofMaternal Prophylaxis

Puerperal sepsis (or ‘‘childbed fever’’) has been associated with maternal morbidity and mortality for centuries. The controversial figure, Ign ac Semmelweiss, a Hungarian obstetrician who practiced in Vienna in the early to mid-1800s, was the first to identify an infectious mode of transmission of puerperal sepsis. Semmelweiss, in a key observation, linked the septic death of a colleague after an autopsy of a woman with puerperal sepsis to an infectious agent in ‘‘decaying matter,’’ a contentious idea at a time when puerperal sepsis was thought to occur solely in women. His observations led to his strong espousal of hand washing before the examination of patients. These speculations of an organic causative agent in puerperal sepsis helped to lay the groundwork for the germ theory of infection several decades later. Group B Streptococcus (Streptococcus agalactiae; GBS) was first identified as a cause of puerperal sepsis in 1935 when Lancefield and Hare observed differences in thehemolytic culture characteristics of two typesof streptococciobtained from autopsies of women who had puerperal sepsis. Fry subsequently reported several cases of fatal puerperal sepsis related to group B streptococcal disease. The use of antibiotics, initially sulfa drugs, followed by penicillin, dramatically decreased mortality attributable to puerperal sepsis. It was not until the early 1960s, however, that an association was observed between GBS infection in mothers and their newborn infants. Subsequent studies showed that although all known GBS serotypes could cause maternal infection, type III was associated with most invasive neonatal disease (meningitis).