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通过连续低水平菌血症诱导实验性心内膜炎,模拟人类自发性菌血症。

Induction of experimental endocarditis by continuous low-grade bacteremia mimicking spontaneous bacteremia in humans.

机构信息

Department of Fundamental Microbiology, Biophore Building, University of Lausanne, CH-1015 Lausanne, Switzerland.

出版信息

Infect Immun. 2011 May;79(5):2006-11. doi: 10.1128/IAI.01208-10. Epub 2011 Feb 14.

DOI:10.1128/IAI.01208-10
PMID:21321073
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3088130/
Abstract

Transient high-grade bacteremia following invasive procedures carries a risk of infective endocarditis (IE). This is supported by experimental endocarditis. On the other hand, case-control studies showed that IE could be caused by cumulative exposure to low-grade bacteremia occurring during daily activities. However, no experimental demonstration of this latter possibility exists. This study investigated the infectivity in animals of continuous low-grade bacteremia compared to that of brief high-grade bacteremia. Rats with aortic vegetations were inoculated with Streptococcus intermedius, Streptococcus gordonii or Staphylococcus aureus (strains Newman and P8). Animals were challenged with 10(3) to 10(6) CFU. Identical bacterial numbers were given by bolus (1 ml in 1 min) or continuous infusion (0.0017 ml/min over 10 h). Bacteremia was 50 to 1,000 times greater after bolus than during continuous inoculation. Streptococcal bolus inoculation of 10(5) CFU infected 63 to 100% vegetations compared to 30 to 71% infection after continuous infusion (P > 0.05). When increasing the inoculum to 10(6) CFU, bolus inoculation infected 100% vegetations and continuous infusion 70 to 100% (P > 0.05). S. aureus bolus injection of 10(3) CFU infected 46 to 57% valves. This was similar to the 53 to 57% infection rates produced by continuous infusion (P > 0.05). Inoculation of 10(4) CFU of S. aureus infected 80 to 100% vegetations after bolus and 60 to 75% after continuous infusion (P > 0.05). These results show that high-level bacteremia is not required to induce experimental endocarditis and support the hypothesis that cumulative exposure to low-grade bacteremia represents a genuine risk of IE in humans.

摘要

侵袭性操作后一过性的高等级菌血症会导致感染性心内膜炎(IE)。这一观点得到了实验性心内膜炎的支持。另一方面,病例对照研究表明,IE 可能是由日常活动中累积的低等级菌血症引起的。然而,目前尚无关于这种可能性的实验证据。本研究比较了连续低等级菌血症和短暂高等级菌血症对动物的感染性,研究使用了携带主动脉赘生物的大鼠,接种了中间链球菌、戈登链球菌或金黄色葡萄球菌(Newman 株和 P8 株)。动物接受 10(3)到 10(6)CFU 的挑战。通过推注(1 分钟内 1 毫升)或连续输注(10 小时内 0.0017 毫升/分钟)给予相同数量的细菌。推注后菌血症的水平比连续接种时高 50 到 1000 倍。链球菌推注 10(5)CFU 感染 63%到 100%的赘生物,而连续输注感染 30%到 71%(P>0.05)。当接种量增加到 10(6)CFU 时,推注接种感染 100%的赘生物,而连续输注感染 70%到 100%(P>0.05)。金黄色葡萄球菌推注 10(3)CFU 感染 46%到 57%的瓣膜。这与连续输注的 53%到 57%的感染率相似(P>0.05)。金黄色葡萄球菌 10(4)CFU 的接种,推注感染 80%到 100%的赘生物,连续输注感染 60%到 75%(P>0.05)。这些结果表明,高等级菌血症并不是诱发实验性心内膜炎所必需的,支持了这样一种假说,即累积暴露于低等级菌血症确实代表了人类感染性心内膜炎的真正风险。

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