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Genetic Differences Between Invasive and Noninvasive Neonatal Group B Streptococcal Isolates

Fluegge, Kirsten MD*; Wons, Juliana*; Spellerberg, Barbara MD, PhD; Swoboda, Sabrina MD; Siedler, Anette PhD; Hufnagel, Markus MD*; Berner, Reinhard MD*

The Pediatric Infectious Disease Journal: December 2011 - Volume 30 - Issue 12 - p 1027–1031
doi: 10.1097/INF.0b013e31822a2a1f
Original Studies

Background: Streptococcus agalactiae, also known as group B streptococcus (GBS), is the most common cause of neonatal sepsis and meningitis. To improve our understanding of the pathogenesis of neonatal GBS sepsis, better knowledge of clonal relatedness and diversity among invasive and noninvasive GBS isolates is critical.

Methods: In a Germany-based study, invasive neonatal GBS isolates were compared with noninvasive isolates from neonates in whom sepsis was suspected, but whose blood cultures were sterile. The comparison was conducted by means of pulsed-field gel electrophoresis and surface protein gene profiling. In addition, multilocus sequence typing was performed on invasive and noninvasive isolates of the most frequent invasive serotype III.

Results: Pulsed-field gel electrophoresis analysis of noninvasive GBS showed a remarkably more diverse fingerprinting pattern than that of invasive isolates. In contrast to invasive strains, noninvasive isolates did not show any clustering. Surface protein gene profiling also showed significantly different distribution patterns between the 2 panels of isolates. Multilocus sequence typing of invasive and noninvasive serotype III isolates revealed the same clonal complexes, but displayed different sequence types (ST); ST-17 was most common (68.6%) among invasive strains, whereas ST-389 (clonal complex-19) was predominant among noninvasive strains (47.8%).

Conclusions: Our results illustrate a large molecular diversity among neonatal noninvasive GBS strains. Invasive strains, however, represent only a small proportion of the noninvasive GBS population. These findings suggest a selection process that prefers more virulent strains during invasion.

Supplemental Digital Content is available in the text.

From the *Center for Pediatrics and Adolescent Medicine, University Medical Center Freiburg, Freiburg, Germany; †Institute for Medical Microbiology and Hygiene, University of Ulm, Ulm, Germany; and ‡Department of Infectious Disease Epidemiology, Robert-Koch-Institute, Berlin, Germany.

Accepted for publication June 20, 2011.

The authors have no funding or conflicts of interest to disclose.

Address for correspondence: Reinhard Berner, MD, Center for Pediatrics and Adolescent Medicine, University Medical Center Freiburg, Mathildenstrasse 1, D-79106 Freiburg, Germany. E-mail:

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© 2011 Lippincott Williams & Wilkins, Inc.