Abstract
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∆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.
Highlights
Streptococcus canis is a Gram-positive beta-hemolytic group G Streptococcus that colonizes the epithelial, respiratory, gastrointestinal, and urogenital surfaces of cats and dogs [1,2,3]
A retrospective study identified S. canis as the causative agent in ~1% of human streptococcal infections, given the reliance of Lancefield classification for group G Streptococcus identification without further speciation, coupled with close interactions between humans and companion animals, it is likely that S. canis human infections are underestimated [22,23]
24 h, mice were vaginally inoculated with 1 × 107 colonyforming units (CFU) WT group B Streptococcus (GBS) COH1, WT S. canis strain G361 or ∆scm mutant suspended in 10 μL of PBS
Summary
Streptococcus canis is a Gram-positive beta-hemolytic group G Streptococcus that colonizes the epithelial, respiratory, gastrointestinal, and urogenital surfaces of cats and dogs [1,2,3]. Knowledge of S. canis virulence factors remains limited, and is largely extrapolated from genetic similarities to the widely-studied group A Streptococcus (S. pyogenes) [12]. In S. pyogenes, the M protein, which is genetically diverse with more than 200 emm types, serves multiple roles in pathogenesis and immune evasion [30]. SCM is a fibrillar surface protein [26] which binds plasminogen [29] and the Fc region of IgGs from multiple species including human, dog, cat, and mouse [31]. We incorporated in vitro and ex vivo human blood component models, together with murine models of S. canis vaginal colonization, systemic infection, and dermal infection to broadly characterize the virulence potential of the zoonotic S. canis vaginal isolate G361, originally isolated from a 40-year-old female, and its isogenic SCM-deficient mutant (G361∆scm)
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