The Long Fox Memorial Lecture delivered in the University of Bristol at the meeting of the Medico-Chirurgical Society on December 9th, 1925 ... by Carey F. Coombs on the ætiology of cardiac disease.

  • Coombs, C. F. (Carey Franklin), 1879-1932.
Date:
[1925?]
Catalogue details

Licence: In copyright

Credit: The Long Fox Memorial Lecture delivered in the University of Bristol at the meeting of the Medico-Chirurgical Society on December 9th, 1925 ... by Carey F. Coombs on the ætiology of cardiac disease. Source: Wellcome Collection.

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    enter the circulation, and therefore the heart, is different. We do not know exactly how the infection gets into the circulation in human rheumatism, but we may surmise that it is not in the form of a single massive dose. If we look again for a moment at the experimental lesions we shall find that something more than injection of a large dose of organisms into the circulation is required if an endocarditis is to be set up ; for if this were all, every such experiment would provoke an endocardial lesion. This is far from being the case. A majority, varying in the hands of different workers, fails to excite any cardiac lesion. Evidently it is necessary that certain conditions favouring infections should also be satisfied. And a little consideration suggests that this is true of the endocarditis lenta of man. It is very unlikely that every breach of the alimentary or bronchial mucous membranes admits streptococci that succeed in infecting the endocardium ; for endocardial lesions of this kind, though commoner than we used to think, are nevertheless rare. I suppose there are not more than ten or twenty cases in a year in Bristol ; yet the surface of mucous membrane that always lies exposed, to the assaults of these bacteria must be at least as large as that of the ground covered by these University buildings. Now, it is ridiculous to suppose that such an area as this is not penetrated thousands of times a year by streptococci. Clearly, then, we have a parallel here with the experiments ; many inoculations, but few endocardial infections. And in this case we know more of the conditions favouring endocardial infection than we do in that of the rabbits. In the first place, we know that old endocardial faults, whether developmental or acquired, invite new endocardial infections. Again, it was