Clinical lectures on circulatory affections. Lecture 3. On acute endocarditis / by G. A. Gibson.

  • Gibson George Alexander, 1854-1913.
Date:
1900
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Licence: In copyright

Credit: Clinical lectures on circulatory affections. Lecture 3. On acute endocarditis / by G. A. Gibson. Source: Wellcome Collection.

Provider: This material has been provided by the Royal College of Physicians of Edinburgh. The original may be consulted at the Royal College of Physicians of Edinburgh.

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    Sometimes only one form of organism is present in any given case, but in a considerable proportion of instances of the disease mixed infection has occurred. Many interesting questions arise as regards the manner in which the micro-organisms attack the endocardium. It must be remembered that the valves differ in respect of their vas- cularity; while the great venous valves of the heart are freely supplied with blood vessels, the cusps guarding the arterial orifices are destitute of them, unless some previous lesion has led to their development. It therefore follows that endocarditis, when occur- ring primarily, as in the case which has just been brought before you, on the aortic cusps, must be due to poisons circulating in the blood flowing over the surface of these cusps, and not brought to them by nutrient blood vessels. An important consideration bear- ing upon this subject is that advanced by Washbourn. The endothelial cells of the vascular system are really phagocytes, capable of englobing bacteria passing along in the circulation. Washbourn quotes the statement of Metchnikoff, that these endo- thelial cells in fish have their origin in the motile cells on the surface of the yolk sac; hence it is no wonder that they preserve some traces of their ancient activity. That this is true has been clearly proved as regards the blood vessels, and there can be no doubt that the endothelial cells of the heart are endowed with similar functions. In exercising their protective influence by destroying bacteria, these endothelial cells, however, may suffer and give rise to phlebitis or arteritis or endocarditis. Much work has been done in order to ascertain how organisms can produce endocarditis. Klebs announced his belief in the infection of the endocardium by organisms circulating in the blood and acting directly upon the endothelial surface, while Roster expressed his opinion that the organisms were conveyed by the blood vessels into the endocardium, where they acted by embolic processes. As has just been shown, this view does not account for a primary affection of those arterial valves which are destitute of blood vessels. Wyssokowitsch found that wounding valves by means of a sterilised instrument did not give rise to endocarditis, while the injection of pyogenic organisms into a vein after wound- ing the cardiac valves gave rise to acute endocarditis. Ribbert went beyond this observation, and showed that the introduction of such pyogenic organisms by means of a vein, without previous injury to the cusps, was a sufficient cause of endocarditis. Since the publication of his results, they have been frequently verified by other observers. The earliest anatomical change in the development of acute endocardial lesions is the invasion of the endothelial and sub- endothelial layers by the bacteria of the blood in the cardiac cavities, and this, as has been already remarked, may be regarded as a beautiful example of phagocytic activity. Retrogressive