Journal
MICROORGANISMS
Volume 9, Issue 1, Pages -Publisher
MDPI
DOI: 10.3390/microorganisms9010183
Keywords
Streptococcus canis; M protein; virulence factor; innate immunity; vaginal colonization
Categories
Funding
- NIH [1 R01 AI154149]
- UC Chancellor's postdoctoral fellowship
- Hartwell Foundation postdoctoral fellowship
- American Urological Association
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The study investigated the virulence potential of Streptococcus canis, concluding that the SCM protein has modest contribution to invasive disease in murine models, but may contribute to mucosal persistence, highlighting the genetic diversity of SCM.
Streptococcus canis is a common colonizing bacterium of the urogenital tract of cats and dogs that can also cause invasive disease in these animal populations and in humans. Although the virulence mechanisms of S. canis are not well-characterized, an M-like protein, SCM, has recently identified been as a potential virulence factor. SCM is a surface-associated protein that binds to host plasminogen and IgGs suggesting its possible importance in host-pathogen interactions. In this study, we developed in vitro and ex vivo blood component models and murine models of S. canis vaginal colonization, systemic infection, and dermal infection to compare the virulence potential of the zoonotic S. canis vaginal isolate G361 and its isogenic SCM-deficient mutant (G361 increment scm). We found that while S. canis establishes vaginal colonization and causes invasive disease in vivo, the contribution of the SCM protein to virulence phenotypes in these models is modest. We conclude that SCM is dispensable for invasive disease in murine models and for resistance to human blood components ex vivo, but may contribute to mucosal persistence, highlighting a potential contribution to the recently appreciated genetic diversity of SCM across strains and hosts.
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