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表皮葡萄球菌引起的实验性心内膜炎中的细菌浓度相关性

Bacterial concentration correlations in experimental endocarditis caused by Staphylococcus epidermidis.

作者信息

Baddour L M, Christensen G D, Bisno A L

出版信息

J Clin Microbiol. 1987 Feb;25(2):207-10. doi: 10.1128/jcm.25.2.207-210.1987.

Abstract

Using 13 strains of Staphylococcus epidermidis to produce catheter-induced experimental endocarditis in rats, we found that bacterial concentrations in blood cultures obtained at the time of sacrifice correlated significantly with the number of organisms per gram of endocardial vegetation (P less than 0.001) and the total number of organisms per vegetation (P less than 0.001). Furthermore, blood culture concentrations correlated with vegetation weights (P less than 0.001) and sizes of infecting inocula (P less than 0.0001). Mean bacterial concentrations in vegetations more than doubled as bacterial concentrations in blood rose from less than 10 to greater than 100 CFU/ml. Mean values for vegetation weights, total organisms per vegetation, and sizes of infecting inocula were also reflected by the intensity of bacteremia. Moreover, intracardiac catheters were more likely colonized as bacterial concentrations in blood cultures increased, with all catheters culture positive in the 25 animals that exhibited high-grade bacteremia (greater than or equal to 100 CFU/ml). Slime production by the bacteria did not influence the above-mentioned correlations. These data indicate that the blood concentration of bacteria reflects the microbiologic status of infected vegetations in experimental infective endocarditis.

摘要

我们使用13株表皮葡萄球菌在大鼠中制造导管诱导的实验性心内膜炎,发现处死时获得的血培养中的细菌浓度与每克心内膜赘生物中的微生物数量(P<0.001)以及每个赘生物中的微生物总数(P<0.001)显著相关。此外,血培养浓度与赘生物重量(P<0.001)和感染接种物大小(P<0.0001)相关。随着血中细菌浓度从低于10 CFU/ml升至高于100 CFU/ml,赘生物中的平均细菌浓度增加了一倍多。赘生物重量、每个赘生物的微生物总数以及感染接种物大小的平均值也反映了菌血症的强度。此外,随着血培养中的细菌浓度增加,心内导管更易被定植,在表现为高度菌血症(大于或等于100 CFU/ml)的25只动物中,所有导管培养均为阳性。细菌产生的黏液并不影响上述相关性。这些数据表明,细菌的血浓度反映了实验性感染性心内膜炎中受感染赘生物的微生物学状态。

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Natural history of aortic valve endocarditis in rats.大鼠主动脉瓣心内膜炎的自然病史。
Infect Immun. 1982 Jul;37(1):127-31. doi: 10.1128/iai.37.1.127-131.1982.

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