Role of Streptococcus uberis adhesion molecule in the pathogenesis of Streptococcus uberis mastitis.

Abstract Adherence to and internalization into mammary epithelial cells are central mechanisms in the pathogenesis of S. uberis mastitis. Through these pathogenic strategies, S. uberis reaches an intracellular environment where humoral host defenses and antimicrobials in milk are essentially ineffective, thus allowing persistence of this pathogen in the mammary gland. We reported that S. uberis expresses a surface adhesion molecule (SUAM) that has affinity for lactoferrin (LF) and a central role adherence to and internalization of S. uberis into bovine mammary epithelial cells. To define the role of SUAM in the pathogenesis of S. uberis mastitis, we created a sua gene deletion mutant clone of S. uberis UT888 (Δ sua S. uberis UT888) unable to express SUAM. When tested in vitro, Δ sua S. uberis UT888 was defective in adherence to and internalization into bovine mammary epithelial cells. To prove that the absence of SUAM reduces bacterial attachment, subsequent colonization and infection of bovine mammary glands, the wild type S. uberis UT888 and its isogenic Δ sua S. uberis UT888 were infused into mammary quarters of dairy cows. Results showed that fewer mammary glands infused with Δ sua S. uberis UT888 become infected than those infused with the isogenic parental strain. Furthermore, mammary glands infused with Δ sua S. uberis UT888 had less severe clinical symptoms as compared to those infused with the isogenic parental strain. These results suggest that the SUAM mutant clone was less virulent than the isogenic parental strain which further substantiates the role of SUAM in the pathogenesis of S. uberis mastitis.