Hagberg L, Engberg I, Freter R, Lam J, Olling S, Svanborg Edén C
Infect Immun. 1983 Apr;40(1):273-83. doi: 10.1128/iai.40.1.273-283.1983.
A model for ascending unobstructed urinary tract infection was developed in mice to study the pathogenesis of urinary tract infection induced by Escherichia coli associated with urinary tract infection in humans. Specifically, the model was designed to monitor the initial stages of the infectious process, e.g., bacterial adhesion. Mice were selected since the specificity and intensity of bacterial attachment of pyelonephritogenic E. coli strains to human and mouse uroepithelial cells were similar. Female mice were infected by urethral catheterization and installation of bacteria in the urinary bladder. To maximize clearance of unattached bacteria, no obstructive manipulations were performed. After sacrifice, the persistence of bacteria in kidneys and bladder was determined by viable counts on homogenized tissues. The experimental infection was standardized by using one pyelonephritis (HU734) and one normal fecal (414) E. coli isolate. With both strains all of the bladders became infected, but E. coli 414 was eliminated more rapidly than HU734. The percentage of positive kidney cultures increased with the bacterial inoculum concentration and volume. An inoculum of 0.05 ml containing 10(10) bacteria per ml was selected, giving the highest percentage of positive kidney cultures without detectable bacterial spread to the blood stream. The variation in the percentage of positive kidney cultures possibly depended on the degree of vesicoureteric reflux in the individual animals. Both in the kidneys and in the urinary bladders, strain HU734 yielded higher numbers of bacteria at 24 h and persisted longer than did strain 414. Several E. coli pyelonephritis isolates with properties associated with virulence in the human urinary tract consistently were recovered from mouse kidneys and bladders in higher numbers than E. coli strains of human fecal origin lacking those properties. The role of bacterial adhesion per se is the topic of the accompanying paper.
为了研究与人类尿路感染相关的大肠杆菌引起的尿路感染的发病机制,在小鼠中建立了上行性无梗阻尿路感染模型。具体而言,该模型旨在监测感染过程的初始阶段,例如细菌黏附。选择小鼠是因为致肾盂肾炎的大肠杆菌菌株对人和小鼠尿路上皮细胞的细菌附着特异性和强度相似。通过尿道插管并将细菌注入膀胱来感染雌性小鼠。为了最大程度地清除未附着的细菌,未进行梗阻性操作。处死后,通过对匀浆组织进行活菌计数来确定肾脏和膀胱中细菌的持久性。使用一株肾盂肾炎大肠杆菌(HU734)和一株正常粪便大肠杆菌(414)分离株使实验感染标准化。两种菌株感染后所有膀胱均被感染,但大肠杆菌414比HU734清除得更快。肾脏培养阳性的百分比随细菌接种物浓度和体积的增加而增加。选择每毫升含10(10)个细菌的0.05毫升接种物,该接种物在肾脏培养阳性百分比最高的同时,未检测到细菌扩散至血流。肾脏培养阳性百分比的差异可能取决于个体动物的膀胱输尿管反流程度。在肾脏和膀胱中,菌株HU734在24小时时产生的细菌数量更多,并且比菌株414持续存在的时间更长。与人类尿路毒力相关的几种大肠杆菌肾盂肾炎分离株,从小鼠肾脏和膀胱中回收的数量始终高于缺乏这些特性的人类粪便来源的大肠杆菌菌株。细菌黏附本身的作用是随附论文的主题。