Manning J E, Hume E B, Hunter N, Knox K W
Institute of Dental Research, United Dental Hospital, Sydney NSW, Australia.
J Med Microbiol. 1994 Feb;40(2):110-4. doi: 10.1099/00222615-40-2-110.
Platelet aggregation is believed to be a virulence factor in infective endocarditis. Other factors may be adhesion to components of thrombotic vegetations, particularly platelets, fibronectin and fibrinogen. Two strains from the Streptococcus sanguis group (SSG) were chosen for comparative study on the basis that one aggregated both human and rat platelets and the other lacked this capacity. Both strains caused endocarditis in the rat model but the aggregating strain was found in higher numbers in the excised vegetations. The nonaggregating strain was unable to bind to human or rat platelets but could bind insoluble fibronectin, insoluble fibrinogen and platelet-fibrin clots from both sources, albeit to a lesser extent than the aggregating strain. These results suggest that whereas adhesion to, and aggregation of, platelets are not essential events in the initiation of the pathogenesis of experimental endocarditis, they may be factors contributing to virulence.
血小板聚集被认为是感染性心内膜炎的一个毒力因子。其他因素可能是对血栓性赘生物成分的黏附,特别是血小板、纤连蛋白和纤维蛋白原。从血链球菌组(SSG)中选择了两株菌株进行比较研究,依据是一株能使人类和大鼠血小板聚集,而另一株缺乏这种能力。两株菌株在大鼠模型中均引发了心内膜炎,但在切除的赘生物中发现聚集菌株的数量更多。非聚集菌株无法与人或大鼠血小板结合,但能结合不溶性纤连蛋白、不溶性纤维蛋白原以及来自这两种来源的血小板 - 纤维蛋白凝块,尽管程度低于聚集菌株。这些结果表明,虽然对血小板的黏附和聚集并非实验性心内膜炎发病机制起始阶段的必要事件,但它们可能是导致毒力的因素。