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Bacterial Infections

The Impact of Circulating Antibody on Group B Streptococcus Intestinal Colonization and Invasive Disease

Michelle J. Vaz, Sheryl A. Purrier, Maryam Bonakdar, Anna B. Chamby, Adam J. Ratner, Tara M. Randis
Denise Monack, Editor
Michelle J. Vaz
aDepartment of Pediatrics, NYU School of Medicine, New York, New York, USA
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Sheryl A. Purrier
bDepartment of Pediatrics, Yale School of Medicine, New Haven, Connecticut, USA
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Maryam Bonakdar
cPathobiology Graduate Program, Brown University, Providence, Rhode Island, USA
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Anna B. Chamby
dThe University of Vermont, Larner College of Medicine, Burlington, Vermont, USA
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Adam J. Ratner
aDepartment of Pediatrics, NYU School of Medicine, New York, New York, USA
eDepartment of Microbiology, NYU School of Medicine, New York, New York, USA
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Tara M. Randis
fDepartment of Pediatrics, University of South Florida, Tampa, Florida, USA
gDepartment of Molecular Medicine, University of South Florida, Tampa, Florida, USA
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Denise Monack
Stanford University
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DOI: 10.1128/IAI.00348-20
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ABSTRACT

Gastrointestinal (GI) colonization with group B Streptococcus (GBS) is an important precursor to late-onset (LO) disease in infants. The host-pathogen interactions that mediate progression to invasive disease remain unknown due, in part, to a paucity of robust model systems. Passively acquired maternal GBS-specific antibodies protect newborns from early-onset disease, yet their impact on GI colonization and LO disease is unexplored. Using murine models of both perinatal and postnatal GBS acquisition, we assessed the kinetics of GBS GI colonization, progression to invasive disease, and the role of GBS-specific IgG production in exposed offspring and juvenile mice at age 12 and 14 days, respectively. We defined LO disease as >7 days of life in the perinatal model. We studied the impact of maternal immunization using a whole-cell GBS vaccine on the duration of intestinal colonization and progression to invasive disease after postnatal GBS exposure in offspring. Animals exhibit sustained GI colonization following both perinatal and postnatal exposure to GBS, with 21% and 27%, respectively, developing invasive disease. Intestinal colonization with GBS induces an endogenous IgG response within 20 days of exposure. Maternal vaccination with whole-cell GBS induces production of GBS-specific IgG in dams that is vertically transmitted to their offspring but does not decrease the duration of GBS intestinal colonization or reduce LO mortality following postnatal GBS exposure. Both perinatal and postnatal murine models of GBS acquisition closely recapitulate the human disease state, in which GBS colonizes the intestine and causes LO disease. We demonstrate both endogenous production of anti-GBS IgG in juvenile mice and vertical transfer of antibodies to offspring following maternal vaccination. These models serve as a platform to study critical host-pathogen interactions that mediate LO GBS disease.

FOOTNOTES

    • Received 13 June 2020.
    • Returned for modification 6 August 2020.
    • Accepted 1 October 2020.
    • Accepted manuscript posted online 19 October 2020.
  • Supplemental material is available online only.

  • Copyright © 2020 American Society for Microbiology.

All Rights Reserved.

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The Impact of Circulating Antibody on Group B Streptococcus Intestinal Colonization and Invasive Disease
Michelle J. Vaz, Sheryl A. Purrier, Maryam Bonakdar, Anna B. Chamby, Adam J. Ratner, Tara M. Randis
Infection and Immunity Dec 2020, 89 (1) e00348-20; DOI: 10.1128/IAI.00348-20

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The Impact of Circulating Antibody on Group B Streptococcus Intestinal Colonization and Invasive Disease
Michelle J. Vaz, Sheryl A. Purrier, Maryam Bonakdar, Anna B. Chamby, Adam J. Ratner, Tara M. Randis
Infection and Immunity Dec 2020, 89 (1) e00348-20; DOI: 10.1128/IAI.00348-20
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    • ABSTRACT
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KEYWORDS

Streptococcus agalactiae (group B Streptococcus [GBS])
late-onset sepsis
neonates
antibody

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