CAMP factor is not essential for systemic virulence of Group B Streptococcus

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Updated: Jul 11, 2026

A Murine Model of Group B Streptococcus Vaginal Colonization
10:19

A Murine Model of Group B Streptococcus Vaginal Colonization

Published on: November 16, 2016

Mary E Hensler1, Darin Quach, Chia-Jun Hsieh

  • 1Division of Pediatric Pharmacology and Drug Discovery, School of Medicine, University of California-San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0687, USA.

Microbial Pathogenesis
|September 18, 2007
PubMed

Insights

Group B Streptococcus (GBS) produces CAMP factor, a toxin not essential for GBS virulence. Deleting the CAMP factor gene did not affect GBS

Area of Science:

  • Microbiology
  • Pathogenesis
  • Bacterial toxins

Background:

  • Group B Streptococcus (GBS) is a major cause of neonatal bacterial infections.
  • CAMP factor is a GBS-produced pore-forming toxin that exhibits synergistic hemolysis with Staphylococcus aureus beta-toxin.
  • The role of CAMP factor in GBS pathogenesis remains incompletely understood.

Purpose of the Study:

  • To investigate the contribution of CAMP factor to the virulence of GBS.
  • To determine if CAMP factor is essential for GBS systemic infection.

Main Methods:

  • Genetic manipulation: precise allelic replacement was used to delete the cfb gene encoding CAMP factor, creating an isogenic GBS Deltacfb mutant.
  • In vitro assays: phagocyte resistance and endothelial cell invasiveness were assessed.
  • In vivo assays: a mouse model of infection was employed to evaluate virulence.

Main Results:

  • The GBS Deltacfb mutant exhibited equivalent resistance to phagocytosis compared to wild-type GBS.
  • The mutant strain showed similar invasiveness against endothelial cells as the wild-type strain.
  • In a mouse model, the GBS Deltacfb mutant demonstrated full virulence, comparable to wild-type GBS.

Conclusions:

  • CAMP factor, in its native context, is not essential for the systemic virulence of Group B Streptococcus.
  • The pore-forming toxin does not play a critical role in GBS pathogenesis during systemic infection.
  • Further research may be needed to elucidate the precise role, if any, of CAMP factor in specific GBS infection types or stages.

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