Oliver S P, Almeida R A, Calvinho L F
Department of Animal Science, University of Tennessee, Knoxville 37901-1071, USA.
Zentralbl Veterinarmed B. 1998 Oct;45(8):461-71. doi: 10.1111/j.1439-0450.1998.tb00817.x.
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.
要发生乳房内感染（IMI），可能存在与逃避吞噬防御、细菌快速生长、细菌黏附于上皮细胞以及/或者乳腺组织细菌定植相关的机制。在过去十年间，已鉴定出乳房链球菌的几种潜在毒力因子。其中一些因子与细胞相关，而其他因子则存在于细胞外。提议的乳房链球菌抗吞噬因子包括荚膜、中性粒细胞毒素、M样蛋白和R样蛋白。乳房链球菌激活纤溶酶原已被认为是该菌获取营养以实现最佳细菌生长的重要机制。乳房链球菌产生并释放到细胞外的潜在毒力因子包括透明质酸荚膜、透明质酸酶和乳房链球菌因子。从牛IMI中分离出的乳房链球菌可黏附并侵入乳腺上皮细胞。细菌侵入乳腺上皮细胞需要完整的微丝和从头合成的真核蛋白参与；这一过程似乎是通过受体介导的内吞作用机制发生的。乳房链球菌侵入乳腺上皮细胞也需要从头合成细菌蛋白。此外，乳房链球菌可在乳腺上皮细胞内存活较长时间，而不会丧失活力或损伤真核细胞。需要进一步开展研究，以表征乳房链球菌乳房内感染早期阶段发生的宿主-病原体相互作用，从而增进我们对发病机制的理解，进而有助于开发方法，将与奶牛乳房链球菌乳腺炎相关的生产损失降至最低。
