Department of Medicine and the Douglas Smith Foundation for Medical Research, The University of Chicago, Chicago.
J Exp Med. 1940 Aug 31;72(3):261-74. doi: 10.1084/jem.72.3.261.
A study has been made of the mode of origin of the secondary lesions occurring spontaneously during the course of experimental pneumococcus pneumonia in the dog. It was observed that the primary lesions of dogs exhibiting interlobar spread contained much more edema fluid than did those in which the inflammatory process remained confined to a single lobe. Furthermore, the sequence of spread from lobe to lobe in relation to the anatomical arrangement of the bronchi and the prone position of the animal was such as to suggest that secondary lobe involvement arose as a result of edematous pneumonic exudate flowing into the more dependent bronchial openings. Experiments were undertaken to determine whether pneumococci are constantly being distributed throughout the lung in the experimental disease in varying degree yet produce secondary foci of consolidation only if the microorganisms reach the terminal airways and are retained there through some interference with the normal eliminatory mechanism. Attempts to produce secondary lesions in dogs with non-spreading single lobe involvement, by means of plugging a terminal bronchus of a normal lobe with starch paste or mucin were largely unsuccessful. In only three out of 19 instances did a lesion develop at the site of obstruction. An investigation was then made of the distribution of pneumococci in the lungs of dogs at the height of the pneumonia. In dogs with single lobe lesions pneumococci were recovered from the lesion itself but not from any other part of the peripheral lung tissue, whereas in animals showing spread to other lobes pneumococci were found to be distributed widely throughout the lung in both the apparently normal and the involved lobes. Some of the microscopic sections of the uninvolved parts of the lungs of dogs with metastatic lesions revealed small masses of pneumococcus-containing exudate in the smaller bronchi and terminal airways of otherwise normal tissue. This finding, in conjunction with the detection of beginning inflammatory changes in other areas normal in the gross, would seem to provide direct evidence of the manner in which pneumococci are transferred from the initial lesion to other lobes and highly presumptive evidence for the mode of origin of the secondary lesions.
对实验性肺炎球菌肺炎犬在自然病程中发生的继发性病变的起源方式进行了研究。观察到,发生间质性扩散的犬的原发性病变比仅局限于单个肺叶的炎症过程的病变含有更多的水肿液。此外,从一个肺叶到另一个肺叶的扩散顺序与支气管的解剖排列和动物的俯卧位有关,这表明继发性肺叶受累是由于水肿性肺炎渗出物流入更依赖的支气管开口而引起的。进行了实验,以确定肺炎球菌在实验性疾病中是否不断以不同程度分布在整个肺部,但只有当微生物到达终末气道并因某种原因而被保留在那里,正常的排泄机制受到干扰时,才会产生继发性实变病灶。通过用淀粉糊或粘蛋白堵塞正常肺叶的终末支气管,试图在仅有单一肺叶受累且无扩散的犬中产生继发性病变,但大部分未能成功。在 19 例中仅有 3 例在阻塞部位形成病变。然后,研究了肺炎球菌在肺炎高峰期犬肺中的分布。在仅有单一肺叶病变的犬中,肺炎球菌从病变本身回收,但从未从外周肺组织的任何其他部位回收,而在病变扩散到其他肺叶的动物中,肺炎球菌广泛分布于整个肺,无论是在明显正常的肺叶还是受累的肺叶中。在具有转移性病变的犬的未受累肺部分的一些显微镜切片中,在其他正常组织的较小支气管和终末气道中发现了含有肺炎球菌的渗出物的小团块。这一发现与在大体上正常的其他区域发现炎症变化的开始相结合,似乎为肺炎球菌从初始病变转移到其他肺叶的方式提供了直接证据,并为继发性病变的起源方式提供了高度推测性证据。