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首页> 外文期刊>Infection and immunity >Pathogenesis of respiratory Klebsiella pneumoniae infection in rats: bacteriological and histological findings and metabolic alterations.
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Pathogenesis of respiratory Klebsiella pneumoniae infection in rats: bacteriological and histological findings and metabolic alterations.

机译：大鼠呼吸道肺炎克雷伯菌的发病机理：细菌学和组织学发现以及代谢改变。

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Gram-negative bacterial pneumonias have been increasingly important as nosocomial infections. The following model was developed to study the pathogenesis and evaluate therapy of such infections. Intranasal instillation of rats with a suspension of 5 x 10(6) Klebsiella pneumoniae caused bronchopneumonia with 24 h. Bacteria were isolated from the lungs in large numbers (greater than 10(5) colony-forming units [CFU] for at least 13 days after inoculation. Thereafter, the viable concentration decreased to about 10(3) CFU at 21 days but increased to 10(4) CFU at 25 days. Mortality rarely exceeded 25%. Plasma zinc concentration decreased, and plasma seromucoid, lysozyme, and alpha2-macrofetoprotein increased during respiratory K. pneumoniae infection in rats. There seemed to be a linear relationship between seromucoid concentration and the concentration of K. pneumoniae in the lung expressed in log10 units. Plasma zinc, alpha2-macrofetoprtoein, or lysozyme levels, however, did not change until the concentration of bacteria retrieved fron lungs exceeded 4 to 5 logs, Analysis of blood samples obtained serially from the orbital sinuses revealed that rats that succumbed to infection had significantly higher levels of seromucoid, alpha2-macrofetoprotein, and lysozyme and lower levels of plasma zinc than infected rats that survived. Progressive increases in seromucoid and particularly in lysozyme and alpha2-macrofetoprotein appeared to be predicative of death. It is postulated that the threshold effect observed for alpha2-macrofetoprotein and lysozyme reflect significant damage to lung tissue, and thus these two variables are good indexes of the severity of this infection. We propose that this model may be of value in elucidating the pathogenesis of respiratory K. pneumoniae as well as in assessing various models of therapy.
机译：革兰氏阴性细菌性肺炎作为医院感染已变得越来越重要。开发了以下模型来研究此类感染的发病机理和评估治疗方法。鼻内滴注5 x 10（6）肺炎克雷伯菌肺悬液致大鼠支气管肺炎持续24小时。接种后至少13天从肺中分离出大量细菌（大于10（5）集落形成单位[CFU]。此后，在21天时，存活浓度降低至约10（3）CFU，但增加至25天时10（4）CFU。死亡率在呼吸道肺炎克雷伯菌感染期间血浆锌浓度降低，血浆血清类固醇，溶菌酶和α2-甲基甲胎蛋白增加，血清类固醇浓度之间似乎呈线性关系肺中的肺炎克雷伯氏菌浓度以log10单位表示，血浆锌，α2-宏铁蛋白或溶菌酶水平直到肺部细菌回收的细菌浓度超过4至5 log才发生变化。眼眶鼻窦的一系列研究显示，死于感染的大鼠的血清类固醇，α2-甲胎蛋白和溶菌酶水平明显高于正常人，而血浆锌水平却低于正常水平。存活的被感染的大鼠。血清类固醇，尤其是溶菌酶和α2-宏蛋白的逐渐增加似乎是死亡的预兆。据推测，观察到的α2-宏铁蛋白和溶菌酶的阈值效应反映出对肺组织的显着损害，因此这两个变量是该感染严重程度的良好指标。我们建议该模型可能对阐明呼吸道肺炎克雷伯菌的发病机理以及评估各种治疗模型具有价值。

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