Calvinho L F, Almeida R A, Oliver S P
Department of Animal Science, University of Tennessee, Knoxville 37901-1071, USA.
Vet Microbiol. 1998 Mar 15;61(1-2):93-110. doi: 10.1016/s0378-1135(98)00172-2.
Mastitis caused by environmental pathogens is a major problem that affects many well-managed dairy herds. Among the environmental pathogens, Streptococcus dysgalactiae is isolated frequently from intramammary infections during lactation and during the nonlactating period. In spite of its high prevalence, little is known about factors that contribute to the virulence of S. dysgalactiae. During the last decade, several cell-associated and extracellular factors of S. dysgalactiae have been identified; yet, the relative importance of these factors in the transmission and pathogenesis of mastitis caused by S. dysgalactiae has not been defined. Streptococcus dysgalactiae can interact with several plasma and extracellular host-derived proteins such as immunoglobulin G, albumin, fibronectin, fibrinogen, collagen, vitronectin, plasminogen, and alpha 2-macroglobulin. These interactions are mediated by bacterial surface proteins. This organism also produces hyaluronidase and fibrinolysin which may be involved in promoting dissemination of the organism into host tissue. Streptococcus dysgalactiae adheres to and is internalized by bovine mammary epithelial cells in vitro. Involvement of host cell kinases, intact microfilaments and de novo eukaryotic protein synthesis are required for internalization of S. dysgalactiae into bovine mammary epithelial cells; a process that appeared to occur by a receptor-mediated endocytosis mechanism. However, de novo bacterial protein synthesis was not required for epithelial cell internalization. Furthermore, S. dysgalactiae survived within mammary epithelial cells for extended periods of time without losing viability or damaging the eukaryotic cell. Further research on characterization of host-pathogen interactions that take place during the early stages of mammary gland infection will enhance our understanding of pathogenesis of intramammary infection which may contribute to development of methods to minimize production losses due to mastitis.
由环境病原体引起的乳腺炎是一个影响许多管理良好的奶牛群的主要问题。在环境病原体中，乳房链球菌在泌乳期和非泌乳期的乳房内感染中经常被分离出来。尽管其患病率很高，但对导致乳房链球菌毒力的因素知之甚少。在过去十年中，已经鉴定出乳房链球菌的几种细胞相关和细胞外因子；然而，这些因子在乳房链球菌引起的乳腺炎的传播和发病机制中的相对重要性尚未明确。乳房链球菌可以与几种血浆和细胞外宿主衍生蛋白相互作用，如免疫球蛋白G、白蛋白、纤连蛋白、纤维蛋白原、胶原蛋白、玻连蛋白、纤溶酶原和α2-巨球蛋白。这些相互作用由细菌表面蛋白介导。这种生物体还产生透明质酸酶和纤维蛋白溶酶，它们可能参与促进生物体向宿主组织的扩散。乳房链球菌在体外可粘附并被牛乳腺上皮细胞内化。乳房链球菌内化到牛乳腺上皮细胞中需要宿主细胞激酶、完整的微丝和从头开始的真核蛋白合成；这一过程似乎是通过受体介导的内吞机制发生的。然而，上皮细胞内化不需要细菌从头合成蛋白质。此外，乳房链球菌在乳腺上皮细胞内存活很长时间而不丧失活力或损害真核细胞。对乳腺感染早期发生的宿主-病原体相互作用特征的进一步研究将增进我们对乳房内感染发病机制的理解，这可能有助于开发方法以尽量减少乳腺炎造成的生产损失。
