Host-parasite relationships in experimental pneumonia due to pneumococcus type III.
Host-parasite relationships in experimental pneumonia due to pneumococcus type III.
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DOI：
10.1084/jem.92.1.85
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发表时间：
1950-07-01
期刊：
影响因子：
--
通讯作者：
SMITH MR
中科院分区：
文献类型：
--
作者：
WOOD WB;SMITH MR
实验性肺炎是由一种高毒力的III型肺炎球菌菌株产生的，它在快速生长过程中合成了大量的荚膜多糖。III型肺炎与I型肺炎球菌引起的肺炎的不同之处在于：(a) III型感染的死亡更迅速，(b)局部肺病变感染更严重，(c)即使在其他有效的化疗后，也常见明显的化脓。特殊的组织学技术表明，III型生物的更大致病性主要是由于其荚膜黏液层干扰表面吞噬。在生长过程中从生物体脱落的荚膜多糖在肺病变的某些部位也显示出高浓度。肺泡中多余多糖的清除是由于(a)淋巴引流到局部淋巴结和(b)吞噬作用，特别是巨噬细胞的吞噬作用。讨论了游离碳水化合物与III型肺炎的恶性肿瘤和特征性黏性渗出物的可能关系。由III型感染引起的肺脓肿发生在微生物聚集最多的区域。有证据表明，化脓不是由于III型肺炎球菌特有的坏死性毒性产物，而是由于组织中大量细菌的存活，主要是由黏液层的抗吞噬作用引起的。当缺乏保护性黏液层的中间III型突变体产生肺炎时，在感染过程中会发生向黏液样亲本的回变，并且由于中间生物体的选择性吞噬，黏液样形式最终在肺中占主导地位。从单细胞制剂中培养的转化的中间III型菌株发现了与最大毒力III型菌株相似的突变。
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.