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首页> 美国卫生研究院文献>Infection and Immunity >Role of Staphylococcus aureus coagulase and clumping factor in pathogenesis of experimental endocarditis.
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Role of Staphylococcus aureus coagulase and clumping factor in pathogenesis of experimental endocarditis.

机译：金黄色葡萄球菌凝血酶和凝集因子在实验性心内膜炎发病机制中的作用。

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The pathogenic role of staphylococcal coagulase and clumping factor was investigated in the rat model of endocarditis. The coagulase-producing and clumping factor-producing parent strain Staphylococcus aureus Newman and a series of mutants defective in either coagulase, clumping factor, or both were tested for their ability (i) to attach in vitro to either rat fibrinogen or platelet-fibrin clots and (ii) to produce endocarditis in rats with catheter-induced aortic vegetations. In vitro, the clumping factor-defective mutants were up to 100 times less able than the wild type strain to attach to fibrinogen and also significantly less adherent than the parents to platelet-fibrin clots. Coagulase-defective mutants, in contrast, were not altered in their in vitro adherence phenotype. The rate of in vivo infection was inoculum dependent. Clumping factor-defective mutants produced ca. 50% less endocarditis than the parent organisms when injected at inoculum sizes infecting, respectively, 40 and 80% (ID40 and ID80, respectively) of rats with the wild-type strain. This was a trend at the ID40 but was statistically significant at the ID80 (P < 0.05). Coagulase-defective bacteria were not affected in their infectivity. Complementation of a clumping factor-defective mutant with a copy of the wild-type clumping factor gene restored both its in vitro adherence and its in vivo infectivity. These results show that clumping factor plays a specific role in the pathogenesis of S. aureus endocarditis. Nevertheless, the rate of endocarditis with clumping factor-defective mutants increased with larger inocula, indicating the contribution of additional pathogenic determinants in the infective process.
机译：在心内膜炎大鼠模型中研究了葡萄球菌凝固酶和结块因子的致病作用。测试了产生凝结酶和产生凝集因子的亲本菌株金黄色葡萄球菌纽曼和一系列在凝结酶，凝集因子或两者均缺陷的突变体的能力（i）在体外与大鼠纤维蛋白原或血小板纤维蛋白凝块结合的能力（ii）在导管诱发的主动脉植被的大鼠中产生心内膜炎。在体外，聚集因子缺陷型突变体附着于血纤蛋白原的能力比野生型菌株低多达100倍，并且比亲本对血小板血纤蛋白凝块的附着力也少得多。相比之下，凝固酶缺陷型突变体的体外粘附表型没有改变。体内感染率取决于接种物。聚集因子缺陷型突变体产生约。当以接种量注射时，与亲本微生物相比，心内膜炎少感染50％，分别感染40％和80％（分别为ID40和ID80）的野生型大鼠。这是ID40的趋势，但在ID80上具有统计学意义（P <0.05）。凝固酶缺陷型细菌的感染力不受影响。丛集因子缺陷型突变体与野生型丛集因子基因的副本的互补恢复了其体外粘附和体内感染性。这些结果表明聚集因子在金黄色葡萄球菌心内膜炎的发病机理中起特定作用。然而，随着接种量的增加，具有聚集因子缺陷型突变体的心内膜炎的发生率增加，表明在感染过程中其他致病因素的贡献。

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