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Since the early 1970s, group B Streptococcus (GBS) has been the leading cause of early-onset neonatal sepsis in the United States and many countries worldwide.1 2 Although the gastrointestinal tract is the primary source of genital colonisation, 10–30 per cent of women are colonised with GBS in their birth canal.3 Pregnant women with GBS colonisation are 25 times more likely to deliver an infant with early-onset GBS sepsis than women who are culture negative.4 Affected infants become colonised/infected during labour and delivery and present with respiratory distress or other signs of sepsis in the first 24–48 h of life. In 1996, the Centres for Disease Control in collaboration with representatives from the major physician organisations published initial recommendations for the prevention of early-onset GBS disease.5 Those recommendations were modified in 2002 when universal screening of all pregnant women at 35–37 weeks' gestation and treatment of culture-positive women were recommended.6 By 2003–2004, 85% of women were being screened for colonisation with GBS and more than 80% of colonised women received intrapartum prophylaxis.7 As a result, the incidence of early-onset GBS sepsis has fallen from 1.7/1000 live births (1990 data) to 0.28/1000 live births (2008 data). In the absence of intrapartum prophylaxis, 2% of infants will develop early-onset GBS sepsis. Over the past 25 years, the case death rate has fallen from 25–50% to 4–6%. However, there is ongoing concern that infants are still dying from early-onset GBS sepsis and that decrements in the incidence of early-onset disease have plateaued.
In 2009, the Centres for Disease Control and Prevention (CDC) convened a meeting of physician representatives from the American College of Obstetrics and Gynecology and the American Academy of Paediatrics along with representatives from a number of public health groups, nursing organisations, microbiologists, pharmacologists, epidemiologists, state …
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