Yersin B, Glauser M P, Guze P A, Guze L B, Freedman L R
Research Services, Veterans Administration West Los Angeles Medical Center, California.
Infect Immun. 1988 May;56(5):1273-80. doi: 10.1128/iai.56.5.1273-1280.1988.
Studies were undertaken to investigate the relationship of the sensitivity of Escherichia coli to the bactericidal properties of serum and the ability of different strains to induce and sustain endocardial infection in rats. Strains of E. coli demonstrated different degrees of serum sensitivity, as determined by a method which employed concentrations of serum from 10 to 95% and periods of incubation as long as 24 h. The greater the serum sensitivity of the E. coli strain, the less able it was to initiate infection and the more rapidly it was spontaneously eliminated from established infections. Endocardial infection with E. coli was established by intravenous challenge in rats with polyethylene catheters passing through the aortic valve into the left ventricle. An E. coli strain of low serum sensitivity was used; the initiation of infection depended upon the length of time the catheter had been in place and, in addition, whether the catheter was in place at the time of bacterial challenge. Removal of the catheter permitted spontaneous sterilization of the endocardial vegetations. The time necessary for sterilization was in direct proportion to the length of time the catheter remained in place following bacterial challenge. If the catheter was not removed, sterilization of the endocardial vegetations did not take place. These studies suggest that serum bactericidal activity is an important host defense mechanism, acting to prevent the initiation of endocarditis in the case of highly serum-sensitive E. coli and to sterilize experimentally induced endocarditis in the case of less-serum-sensitive bacteria. The catheter used to induce nonbacterial endocardial vegetations favored the colonization of vegetations by E. coli, and it delayed the spontaneous sterilization of infected vegetations which occurred in relation to the susceptibility of the strain to the bactericidal properties of the serum. This effect of the catheter was not attributable to bacteria remaining viable in its lumen, nor was it attributable to inhibition of the bactericidal capacity of the serum as measured in vitro. Whatever the mechanism responsible for the catheter effect, experimental studies of the evolution of infections established with this technique must take into consideration the duration of catheter placement and whether and for how long it was present before or after inoculation with test bacteria.
开展了多项研究，以调查大肠杆菌对血清杀菌特性的敏感性与不同菌株在大鼠中诱导和维持心内膜感染能力之间的关系。通过一种使用浓度为10%至95%的血清且孵育时间长达24小时的方法测定，大肠杆菌菌株表现出不同程度的血清敏感性。大肠杆菌菌株的血清敏感性越高，其引发感染的能力就越弱，并且从已建立的感染中自发清除的速度就越快。通过将带有聚乙烯导管的大鼠进行静脉内攻击，使导管穿过主动脉瓣进入左心室，从而建立大肠杆菌心内膜感染。使用了一种血清敏感性低的大肠杆菌菌株；感染的起始取决于导管留置的时间长度，此外还取决于在细菌攻击时导管是否在位。移除导管可使心内膜赘生物自发灭菌。灭菌所需的时间与细菌攻击后导管留置的时间长度成正比。如果不移除导管，心内膜赘生物就不会发生灭菌。这些研究表明，血清杀菌活性是一种重要的宿主防御机制，在高血清敏感性大肠杆菌的情况下，它可防止心内膜炎的起始，而在血清敏感性较低的细菌的情况下，它可使实验性诱导的心内膜炎灭菌。用于诱导非细菌性心内膜赘生物的导管有利于大肠杆菌在赘生物上定植，并延迟了与菌株对血清杀菌特性的敏感性相关的感染赘生物的自发灭菌。导管的这种作用既不归因于其管腔内存活的细菌，也不归因于体外测量的血清杀菌能力的抑制。无论导致导管作用的机制如何，用这种技术建立的感染演变的实验研究必须考虑导管放置的持续时间以及在接种测试细菌之前或之后导管是否存在以及存在多长时间。
