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III型肺炎球菌所致实验性肺炎中的宿主-寄生虫关系

Host-parasite relationships in experimental pneumonia due to pneumococcus type III.

作者信息

WOOD W B, SMITH M R

出版信息

J Exp Med. 1950 Jul 1;92(1):85-100. doi: 10.1084/jem.92.1.85.

Abstract

Experimental pneumonia was produced with a highly virulent strain of type III pneumococcus which synthesizes, during rapid growth, large amounts of capsular polysaccharide. The type III pneumonia differed from that caused by pneumococcus I in that (a) death occurred more promptly in the type III infection, (b) the local pulmonary lesion became more heavily infected, and (c) frank suppuration was common even after otherwise effective chemotherapy. The greater pathogenicity of the type III organism was shown by special histologic techniques to be due primarily to its capsular slime layer which interferes with surface phagocytosis. Capsular polysaccharide shed from the organism during growth was also demonstrated in high concentration in certain parts of the pneumonic lesion. Removal of the excess polysaccharide from the alveoli resulted from (a) lymphatic drainage to regional lymph nodes and (b) phagocytosis, particularly by macrophages. The possible relationship of the free carbohydrate to the malignancy and the characteristically viscous exudate of type III pneumonia was discussed. The lung abscesses which resulted from type III infection were observed to occur in those areas in which the maximum number of organisms had accumulated. Evidence was obtained that suppuration was due, not to necrotoxic products peculiar to the type III pneumococcus, but rather to the survival of large numbers of bacteria in the tissues, brought about primarily by the antiphagocytic effect of the slime layer. When pneumonia was produced with an intermediate type III mutant lacking the protective slime layer, back mutation to the mucoid parent occurred during the course of the infection, and the mucoid form eventually predominated in the lung as a result of selective phagocytosis of the intermediate organisms. Similar mutation to the maximally virulent type III form was noted with a transformed intermediate type III strain grown from single cell preparations.

摘要

用一种高毒力的III型肺炎球菌菌株诱发实验性肺炎,该菌株在快速生长过程中合成大量荚膜多糖。III型肺炎与I型肺炎球菌引起的肺炎不同,表现为:(a)III型感染时死亡更迅速;(b)局部肺部病变感染更严重;(c)即使在其他方面有效的化疗后,明显的化脓也很常见。特殊组织学技术表明,III型病原体的更大致病性主要归因于其荚膜黏液层,该层会干扰表面吞噬作用。在肺炎病变的某些部位也检测到高浓度的生长过程中从生物体脱落的荚膜多糖。肺泡中多余多糖的清除源于:(a)向局部淋巴结的淋巴引流;(b)吞噬作用,尤其是巨噬细胞的吞噬作用。讨论了游离碳水化合物与III型肺炎的恶性程度和典型黏性渗出物之间的可能关系。观察到III型感染导致的肺脓肿发生在积聚了最多生物体的区域。有证据表明,化脓不是由于III型肺炎球菌特有的坏死毒性产物,而是由于组织中大量细菌的存活,这主要是由黏液层的抗吞噬作用导致的。当用缺乏保护性黏液层的中间型III型突变体诱发肺炎时,在感染过程中会发生向黏液样亲本的回复突变,由于中间型生物体被选择性吞噬,黏液样形式最终在肺中占主导地位。从单细胞制剂培养的转化中间型III型菌株也出现了类似向最大毒力III型形式的突变。

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