Clinical features and molecular characterization of 109 group B streptococci causing neonatal invasive infections were determined over an 18-month period in France. Sixtyfour percent of the strains were from late-onset infections, and 75% were capsular type III. The hypervirulent clone ST-17 was recovered in 80% of meningitis cases.
G roup B Streptococcus (GBS)is the leading cause of infectious illness among newborns. Invasive infections in neonates can result in pneumonia, sepsis, or meningitis. Early-onset disease (EOD) occurs within the fi rst week. Lateonset disease (LOD) occurs after the fi rst week and accounts for most meningitis cases and deaths (1). Because recommendations for intrapartum antibioprophylaxis (IAP) for mothers in labor at risk for GBS infection have been widely implemented in many countries, the incidence of EOD has declined to <1/1,000 births, but the incidence of LOD has remained unchanged (2). To date, 10 capsular serotypes have been described (Ia, Ib, and II-IX). Among these, serotype III is of particular importance because it is responsible for a substantial proportion of EOD and most cases of . Different studies have suggested that most neonatal invasive diseases and almost all cases of meningitis are caused by a limited number of strains belonging to a homogeneous serotype III clone. This clone is defi ned by multilocus sequence typing (MLST) analyses as ST-17, the so-called highly virulent clone (4-8). However, data available in Europe are limited regarding the distribution of GBS genotypes among invasive isolates recovered from neonates.We describe clinical characteristics, capsular type, and MLST allelic and antimicrobial drug-susceptibility profi les of 109 nonredundant GBS isolates that caused neonatal invasive infections. These isolates were collected during an active surveillance performed in France from May 2006 through December 2007.
The StudyClinical data on 109 infants up to 4 months of age were analyzed. Sepsis was defi ned as GBS bacteremia in the presence of consistent clinical signs and symptoms. Meningitis was diagnosed if GBS was recovered from cerebrospinal fl uid. GBS isolates were identifi ed by using a commercial Lancefi eld group-specifi c latex agglutination test. Capsular typing was performed by a multiplex PCR as described (9), and the hypervirulent ST-17 clone was detected by real-time PCR, as reported (6). Susceptibility testing, antibiograms, and MICs were performed according to Clinical and Laboratory Standards Institute recommendations (www.clsi.org). Antimicrobial drug-resistance genes were detected by using the multiplex PCR as described (10). Statistical analysis was performed according to the Fisher exact and χ 2 tests. A p value of <0.05 was used as the threshold for statistical signifi cance.We studied 109 GBS strains responsible for neonatal invasive infections; 36% (n = 39) and 64% (n = 70) were responsible for EOD and LOD, respectively (Table). Eighty percent of EOD cases occurred during the fi rst 24 hours after birth, with a male:female rati...