ROLE OF STAPHYLOCOCCUS-AUREUS COAGULASE AND CLUMPING FACTOR IN PATHOGENESIS OF EXPERIMENTAL ENDOCARDITIS
ROLE OF STAPHYLOCOCCUS-AUREUS COAGULASE AND CLUMPING FACTOR IN PATHOGENESIS OF EXPERIMENTAL ENDOCARDITIS
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DOI：
10.1128/iai.63.12.4738-4743.1995
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发表时间：
1995-12-01
影响因子：
3.1
通讯作者：
VAUDAUX, P
中科院分区：
文献类型：
--
作者：
MOREILLON, P;ENTENZA, JM;VAUDAUX, P
探讨葡萄球菌凝固酶和凝集因子在大鼠心内膜炎模型中的致病作用。产生凝固酶和凝集因子的亲本金黄色葡萄球菌纽曼菌株和一系列凝固酶、凝集因子或两者都有缺陷的突变体被测试了它们(I)在体外附着于大鼠纤维蛋白原或血小板-纤维蛋白凝块的能力，以及(Ii)在导管诱导的主动脉赘生物大鼠中产生心内膜炎的能力。在体外，凝集因子缺陷突变体附着于纤维蛋白原的能力比野生型菌株低100倍，也明显低于亲本菌株附着于血小板-纤维蛋白凝块的能力。相反，凝固酶缺陷突变体的体外黏附表型没有改变，体内感染率与接种量有关。当接种大小分别为40%和80%(分别为ID40和ID80)的野生型菌株感染大鼠时，聚集因子缺陷突变株产生的心内膜炎比亲本微生物少约50%，这在ID40是一种趋势，但在ID80有统计学意义(P<；凝固酶缺陷菌的感染力不受影响，凝集因子缺陷突变株与野生型凝集因子基因拷贝互补，恢复了凝集因子在体外的黏附和体内的感染性。这些结果表明凝集因子在金黄色葡萄球菌心内膜炎的发病机制中起着特定的作用，然而，随着接种量的增加，凝集因子缺陷突变株的心内膜炎发生率增加，表明其他致病决定因素在感染过程中的作用。
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.