Straus D C, Atkisson D L, Garner C W
Infect Immun. 1985 Dec;50(3):787-95. doi: 10.1128/iai.50.3.787-795.1985.
A Klebsiella pneumoniae serotype 2 strain was examined for its ability to produce extracellular toxic material. The organism was grown to the stationary phase in a defined medium, and the toxic material was isolated by ultrafiltration-ion-exchange chromatography on DEAE-Sephacel and gel filtration chromatography on Sepharose 4B or 2B. It was found to be comprised of 63% capsular polysaccharide, 30% lipopolysaccharide, and 7% protein and possessed a 50% lethal dose (when injected intraperitoneally into mice) of 393 +/- 45 micrograms. The toxicity appeared to be associated with the endotoxin portion of the compound, because boiling for 15 min and exposure to proteolytic enzymes had no effect on the toxicity. However, saponification destroyed the toxicity of the compound. Studies employing radial immunodiffusion examining the sera of mice infected with this organism demonstrated in vivo production of the complex at levels sufficiently high to produce death. When sublethal amounts of this complex were placed in the lungs of specific-pathogen-free mice, the lung pathology observed after 24, 48, and 72 h was similar to the damage caused by an active K. pneumoniae lobar pneumonia. These data indicate that this extracellular toxic compound produced by K. pneumoniae may be responsible for the lethality and lung tissue destruction normally associated with an active lobar pneumonia caused by this organism.
对一株肺炎克雷伯菌2型菌株产生细胞外毒性物质的能力进行了检测。该菌株在特定培养基中培养至稳定期,通过在DEAE - 葡聚糖凝胶上进行超滤 - 离子交换色谱以及在琼脂糖4B或2B上进行凝胶过滤色谱来分离毒性物质。结果发现其由63%的荚膜多糖、30%的脂多糖和7%的蛋白质组成,腹腔注射小鼠时的半数致死剂量为393±45微克。毒性似乎与该化合物的内毒素部分有关,因为煮沸15分钟和暴露于蛋白水解酶对毒性没有影响。然而,皂化作用会破坏该化合物的毒性。采用放射免疫扩散法对感染该菌株的小鼠血清进行检测的研究表明,体内会产生足以导致死亡的高水平复合物。当将亚致死量的这种复合物置于无特定病原体小鼠的肺部时,在24、48和72小时后观察到的肺部病理学变化与由活性肺炎克雷伯菌大叶性肺炎引起的损伤相似。这些数据表明,肺炎克雷伯菌产生的这种细胞外毒性化合物可能是导致该菌引起的活性大叶性肺炎通常所伴有的致死性和肺组织破坏的原因。