For intramammary infections (IMI) to occur, mechanisms associated with avoidance of phagocytic defenses, rapid growth of bacteria, adherence of bacteria to epithelial cells, and/or bacterial colonization of mammary tissue are probably present. During the last decade, several potential virulence factors of Streptococcus uberis have been identified. Some of these factors are cell-associated while other factors are extracellular. Proposed antiphagocytic factors of S. uberis include capsule, neutrophil toxin, M-like protein and R-like protein. Activation of plasminogen by S. uberis has been proposed as an important mechanism for this organism to obtain nutrients for optimal bacterial growth. Potential virulence factors produced by S. uberis and released extracellularly include hyaluronic acid capsule, hyaluronidase and uberis factor. Streptococcus uberis isolated from bovine IMI adhere to and invade mammary epithelial cells. Involvement of intact microfilaments and de novo eukaryotic protein synthesis are required for bacterial invasion of mammary epithelial cells; a process that appeared to occur by a receptor-mediated endocytosis mechanism. De novo bacterial protein synthesis was also required for invasion of S. uberis into mammary epithelial cells. Furthermore, S. uberis survived within mammary epithelial cells for extended periods of time without losing viability or damaging the eukaryotic cell. Further research directed towards characterization of host-pathogen interactions that take place during the early stages of S. uberis intramammary infection are needed to enhance our understanding of pathogenesis and thus contribute to development of methods to minimize production losses associated with S. uberis mastitis in dairy cows.